LncRNA name	Synonyms	geneid	ensg_name	refseq_id	position	cancer type	ICD-0-3	ICD-0-3	methods	sample	regulated	function description	pubmed id	year	title
linc-ROR	LINC-ROR, ROR, lincRNA-RoR	100885779	ENSG00000258609	NR_048536	GRCh38_18:57054558-57072119	endometrial cancer	NA	M8380/3	qPCR, RNAi, Flow cytometry assay, FISH etc.	endometrial carcinoma tissues	up-regulated	We began by assessing the expression of linc-RoR in ECSC growing under tumorsphere conditions and differentiated conditions (removal of bFGF). In qRT-PCR analyses, a marked reduction of linc-RoR and core TFs was observed in all differentiated tumorspheres. This finding suggested that linc-RoR expression was positively correlated with levels of undifferentiated tumorspheres. The effects of miR-145 could be eliminated after increasing the expression of linc-RoR in ETs or mutated targeted sequences in linc-RoR. 	24589415	2014	Linc-RNA-RoR acts as a sponge against mediation of the differentiation of endometrial cancer stem cells by microRNA-145.
NAMA	NAMA	100996569	ENSG00000271086	NR_102270	GRCh38_9:99355337-99377240	papillary thyroid cancer	NA	M8260/3	qPCR, RNAi, RIP, Flow cytometry assay etc.	PTC tissues, cell line (IHH-4)	down-regulated	The expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. 	26323637	2015	BRAF-activated Long Non-coding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor.
CCAT2	CCAT2, LINC00873, NCCP1	101805488	ENSG00000280997	NR_109834	GRCh38_8:127400399-127402150	gastric cancer	C16	NA	qPCR, Western blot etc.	cell lines (BGC-823)	up-regulated	CCAT2 was able to positively regulate the expression of POU5F1B gene. Furthermore, silencing of CCAT2 gene inhibited the proliferation of BGC-823 cells, as well as induced apoptosis and autophagy in BGC-823 cells, by suppression of the PI3K/mTOR signaling pathways.Recent studies confirmed that the lncRNA CCAT2, located at the 8q24 amplicon of the cancer risk-associated rs6983267 SNP, regulated the cancer metabolism in vitro and in vivo by directly interacting in an allele-specific manner with a protein complex. The chromosomal region 8q24 emerged as an important region for genetic susceptibility in various cancer types, thus DNA methylation or SNPs at this locus may contribute to cancer risk. RT-qPCR results revealed that CCAT2 gene expression was effectively suppressed by the transfection, while POU domain class 5 transcription factor 1B (POU5F1B) gene expression was significantly decreased. 	29435046	2017	Effect of silencing colon cancer-associated transcript 2 on the proliferation,apoptosis and autophagy of gastric cancer BGC-823 cells.
ENST00000457390	RP11-14N7.2, LOC100996732	NA	NA	NA	GRCh38_1:144245027-144245821	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	down-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000476909	LINC00856	NA	NA	NA	GRCh38_10:78267410-78280213	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	down-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000553559	SNHG10, C14orf62, LINC00063, NCRNA00063	283596	ENSG00000247092	NR_001459	GRCh38_14:95532914-95534872	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	up-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000565617	KB-1460A1.5	NA	NA	NA	GRCh38_8:101166805-101169629	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	down-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000568031	RP11-863P13.3	NA	NA	NA	GRCh38_16:88177298-88178610	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	up-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
ENST00000576810	RP11-462G12.1, LOC102724927	NA	NA	NA	GRCh38_16:3947609-3950444	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	down-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
EZR-AS1	NA	101409257	ENSG00000233893	NR_102425	GRCh38_6:158818011-158820593	esophageal squamous cell cancer	NA	NA	RNA-seq, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP	esophageal squamous cell carcinoma (ESCC) tissues and cell lines (KYSE150 and KYSE510)	up-regulated	Both in vivo and in vitro studies revealed that EZR-AS1 promoted cell migration through up-regulation of EZR expression. Mechanistically, antisense lncRNA EZR-AS1 formed a complex with RNA polymerase II to activate the transcription of EZR. Moreover, EZR-AS1 could recruit SMYD3 to a binding site, present in a GC-rich region downstream of the EZR promoter, causing the binding of SMYD3 and local enrichment of H3K4me3. Finally, the interaction of EZR-AS1 with SMYD3 further enhanced EZR transcription and expression. Our findings suggest that antisense lncRNA EZR-AS1, as a member of an RNA polymerase complex and through enhanced SMYD3-dependent H3K4 methylation, plays an important role in enhancing transcription of the EZR gene to promote the mobility and invasiveness of human cancer cells.EZR-AS1 regulates EZR transcriptional activity in ESCC cells by interacting with RNA polymerase II, but not by affecting the binding of SP1 and AP-1 transcription factors. the overexpression of EZR-AS1 accompanied the enhanced expression of EZR (variant 1), both at the mRNA and protein levels, in KYSE150 cells (Figure 1H and I). 	29253179	2018	The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells.
FAM83H-AS1	FAM83H-AS1, onco-lncRNA-3	100128338	NA	NR_033849	NA	pancreatic ductal adenocarcinoma	C25.3	M8500/3	RNA-seq, qrT-PCR, Western blot	cell lines (PANC-1 PANC1, BxPC3, MiaPaCa2 and Aspc1)	up-regulated	We identified lncRNAs in genomic regions with SCNA and single nucleotide polymorphisms associated with lifetime risk of PDA and associated with clinical outcome using genomic and clinical data in PDA. Systems biology and experimental functional analysis of two epithelial lncRNAs (LINC00673 and FAM83H-AS1) suggest they regulate the transcriptional profile of pancreatic tumour samples and PDA cell lines.We also detected lncRNAs located in proximity to GATA6 and FOXA2, both important transcription factors involved in pancreas development. PDA is characterised by high penetrance mutations in four genes (KRAS, TP53, CDKN2A and SMAD4). We performed a similar analysis and identified five candidate lncRNAs within loci that harboured somatic SNP variants associated with increased risk of PDA	29440233	2018	Comprehensive characterisation of compartment-specific long non-coding RNAs associated with pancreatic ductal adenocarcinoma.
FAM99A	FAM99A	387742	ENSG00000205866	NR_026643	GRCh38_11:1665597-1667856	hepatocellular carcinoma	C22.0	M8170/3	RNA-seq, qPCR etc.	HCC tissues	down-regulated	We found that LINC01093, FAM99A and CRNDE were differentially expressed in HCC compared with cirrhotic tissues, confirming the data we obtained in the RNA-Seq experiment. Moreover, we found that LINC01093 and FAM99A were already significantly downregulated in cirrhotic tissues compared with normal livers.	26887054	2016	Identification of novel long non-coding RNAs deregulated in hepatocellular carcinoma using RNA-sequencing.
FOXC2-AS1	FOXC2-AS1, ODRUL	103752587	ENSG00000260944	NR_125795	GRCh38_16:86565145-86567761	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	up-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
HOTAIR	HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072	100124700	ENSG00000228630	NR_003716	GRCh38_12:53962308-53974956	colon cancer	C18	NA	qPCR, Western blot, Luciferase reporter assay etc.	cell lines (CCL228, HeLa, MCF7, SH-SY5Y) 	up-regulated	Along with HIF1a, histone methylases MLL1 and histone acetylase p300 are enriched at the HOTAIR promoter under hypoxia. The levels of H3K4-trimethylation and histone acetylation are also enriched at the HOTAIR promoter. Furthermore, knockdown of MLL1 downregulated the hypoxia-induced HOTAIR expression, indicating key roles of MLL1 in hypoxia-induced HOTAIR expression. HIFs are transcription factors and regulate the expression of a variety of target genes under hypoxia and that contribute to the tumor growth and metastasis.Misregulation and mutations in lncRNAs are widely associated with a variety of human diseases.	28756022	2017	Histone methylase MLL1 coordinates with HIF and regulate lncRNA HOTAIR expression under hypoxia.
HOTTIP	HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213	100316868	ENSG00000243766	NR_037843	GRCh38_7:27198575-27207259	pancreatic cancer	C25	NA	qPCR, Luciferase reporter assay	PC cell line, PC tissues.	down-regulated	The current findings provided evidence that the functional rs1859168 A > C polymorphism may decrease the PC risk by down-regulating the HOTTIP expression.In addition, functional prediction of SNP revealed that rs1859168 could alter HOTTIP expression by influencing the transcription factor binding sites, and HOTTIP takes part in regulating cancer cell proliferation and survival [29, 30, 31]. In addition, functional prediction of SNP revealed that rs1859168 could alter HOTTIP expression by influencing the transcription factor binding sites, and HOTTIP takes part in regulating cancer cell proliferation and survival [29, 30, 31].	28818070	2017	rs1859168 A>C polymorphism regulates HOTTIP expression and reduces risk of pancreatic cancer in a Chinese population.
LCAL1	LCAL1, onco-lncRNA-27	80078	NA	NR_130915	NA	lung cancer	C34	NA	RNA-seq, qPCR, RNAi etc.	lung cancer tissues	up-regulated	Stable overexpression of LCAL1, using two different clones, in the control cell line BEAS-2B showed a significant increase in cellular proliferation starting on day 2 and continuing until the end of the experiment at day 6 with a 38% and 43% growth increase, respetcively. Overexpression of LCAL1 in normal BEAS-2B cells is proof of principle that this lncRNA is sufficient to affetc cellular growth independently of other common cancer mutations, thus highlighting the importance of LCAL1 in lung cancer biology.	25116943	2014	Transcriptome sequencing reveals altered long intergenic non-coding RNAs in lung cancer.
LINC00673	LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1	100499467	NA	NR_036488	GRCh38_17:72403322-72592804	pancreatic ductal adenocarcinoma	C25.3	M8500/3	RNA-seq, qPCR, Western blot	cell lines (PANC-1 PANC1, BxPC3, MiaPaCa2 and Aspc1,)	up-regulated	We generated a catalogue of PDA-associated lncRNAs. Systems biology and experimental functional analysis of two epithelial lncRNAs (LINC00673 and FAM83H-AS1) suggest they regulate the transcriptional profile of pancreatic tumour samples and PDA cell lines.We also detected lncRNAs located in proximity to GATA6 and FOXA2, both important transcription factors involved in pancreas development. PDA is characterised by high penetrance mutations in four genes (KRAS, TP53, CDKN2A and SMAD4).We performed a similar analysis and identified five candidate lncRNAs within loci that harboured somatic SNP variants associated with increased risk of PDA	29440233	2018	Comprehensive characterisation of compartment-specific long non-coding RNAs associated with pancreatic ductal adenocarcinoma.
lincRNA-p21	TP53COR1, TRP53COR1, linc-p21, lincRNA-p21	102800311	NA	NA	NA	glioma	NA	M9380/3	qPCR, Western blot etc.	cell lines (SMMC7721, U251MG)	down-regulated	In this work, we found that X-ray irradiation or hypoxia treatment elevated lincRNA-p21 expression in SMMC7721 hepatoma and U251MG glioma  cells.High lincRNA-p21 levels were associated with poor cancer-specific survival in patients. F.. However, tumor cells can express a wide range of transcription factors, such as hypoxia-inducible factor-1a (HIF-1a).found that LincRNA-p21 was downregulated in non-small-cell lung cancer tissue, but no association was observed with TP53 mutational status. 	28689810	2017	LincRNA-p21 knockdown enhances radiosensitivity of hypoxic tumor cells by reducing autophagy through HIF-1/Akt/mTOR/P70S6K pathway.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	pancreatic neuroendocrine tumor	C25	M8246/3	microarray, qPCR, Luciferase reporter assay etc.	pancreatic neuroendocrine tumors tissues, cell lines (MIN6 and MIN6-4N)	down-regulated	We found that Meg3 has tumor-suppressor activity in PNET cells because the overexpression of Meg3 in MIN6 cells (insulin-secreting mouse PNET cell line) blocked cell proliferation and delayed cell cycle progression. Gene expression microarray analysis showed that Meg3 overexpression in MIN6 mouse insulinoma cells down-regulated the expression of the protooncogene c-Met (hepatocyte growth factor receptor), and these cells showed significantly reduced cell migration/invasion. Compared with normal islets, mouse or human MEN1-associated PNETs expressed less MEG3 and more c-MET	25565142	2015	Epigenetic regulation of the lncRNA MEG3 and its target c-MET in pancreatic neuroendocrine tumors
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	hepatocellular carcinoma	C22.0	M8170/3	microarray, qPCR, Western blot, RIP, Flow cytometry assay, RNA pull-down assay etc.	HCC tissues, cell lines (HepG2, SK-Hep-1, HEK293, HCT116)	down-regulated	Our results demonstrate for the first time that MEG3 can interact with p53 DNA binding domain and various p53 target genes are deregulated after overexpression of MEG3 in hepatoma cells. Furthermore, results of qRT-PCR have shown that MEG3 RNA is lost or reduced in the majority of HCC samples compared with adjacent non-tumorous samples. Ectopic expression of MEG3 in hepatoma cells significantly inhibits proliferation and induces apoptosis.	26444285	2015	Long Noncoding RNA MEG3 Interacts with p53 Protein and Regulates Partial p53 Target Genes in Hepatoma Cells.
MVIH	AK094613	NA	NA	NA	NA	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Western blot, etc.	Hepatoma cell line HepG2, liver tumor-derived cell lines SKHEP-1, Huh7	up-Regulated	Our data suggests that deficiency or loss of functional mutations of ARID1A in HCC cells might contribute to the increased activity ofcertain cancer-promoting lncRNAs。AIRD1A fragments (A-1, aa 1e310; A-2, aa 311e600; A-3, aa 601e950; A-4, aa 951e1300; A-5, aa 1301e1600; A-6, aa 1601e1900; A-7, aa 1901e2285) were amplified by PCR and subcloned into pGEX-4T-1 vectors (GE Healthcare Life Sciences) to generate recombinant GST-ARID1A fusion proteins. As a subunit of SWI/SNF complex, ARID1A could contribute to its chromatin remodeling activity by recruiting and binding of specific transcription factor and transcriptional coactivator/corepressor complexes.ARID1A, encoding the BAF250a subunit of SWI/SNF complex, has a high mutation frequency in numerous types of cancer. 	28716731	2017	ARID1A represses hepatocellular carcinoma cell proliferation and migration through lncRNA MVIH.
NR_033878	LINC00944	387895	ENSG00000256128	NR_033878	GRCh38_12:126752164-126761045	osteosarcoma	NA	M9180/3	microarray, qPCR, MTT assay etc.	cell line (MG63/DXR)	up-regulated	The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls.	26464619	2015	Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis.
PCAT29	PCAT29	104472713	ENSG00000259641	NR_126437	GRCh38_15:69592200-69695750	prostate cancer	C61.9	NA	qPCR, Western blot etc.	cell lines (VCap, PC3M-luc, LNCaP etc.)	down-regulated	This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAIC and PCAT30, that are prognostic for a wide variety of cancer types.This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAICand PCAT29, that are prognostic for a wide variety of cancer types.	25700553	2015	The lncRNA DRAIC/PCAT29 locus constitutes a tumor suppressive nexus.
PRNCR1	PRNCR1, CARLo-3, PCAT8	101867536	ENSG00000282961	NR_109833	GRCh38_8:127079874-127092600	gastric cancer	C16	NA	qPCR etc.	gastric cancer tissues	differential expression	We found that patients with the rs13252298AG genotype displayed a 1.50-fold increased risk of GC. Interestingly, the rs7007694CT and CC and the rs1456315GG genotypes displayed a decreased risk of GC. Our results suggest that SNPs in the lncRNA PRNCR1 may be a biomarker for the etiology of GC	26206497	2015	Association between polymorphisms in long non-coding RNA PRNCR1 in 8q24 and risk of gastric cancer
PTCSC2	NA	101928337	ENSG00000236130	NR_147055	GRCh38_9:97805935-97810008	thyroid cancer	C73.9	NA	RIP, Dual-luciferase reporter assay, RNA pull-down assay etc.	thyroid cancer tissues, cell lines (KTC1, BCPAP, C643, SW1736, TPC1, FTC133)	differential expression	Here we report that PTCSC2 binds myosin-9 (MYH9). In a bidirectional promoter shared by FOXE1 and PTCSC2, MYH9 inhibits the promoter activity in both directions. This inhibition can be reversed by PTCSC2, which acts as a suppressor. RNA knockdown of FOXE1 in primary thyroid cells profoundly interferes with the p53 pathway. We propose that the interaction between the lncRNA, its binding protein MYH9, and the coding gene FOXE1 underlies the predisposition to PTC triggered by rs965513.	28049826	2017	MYH9 binds to lncRNA gene PTCSC2 and regulates FOXE1 in the 9q22 thyroid cancer risk locus.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	lung cancer	C34	NA	qPCR, Luciferase reporter assay etc.	cell lines (A549, 95D, HCC827, NCI-H1650)	up-regulated	YY1 could directly bind to the promoter region of (long noncoding RNAplasmacytoma variant translocation 1 [lncRNA-PVT1]) and activated its transcription through the consensus YY1 motif. Knockdown of the expression of YY1 reduced cell proliferation in vivo, consistent with the results obtained from silencing the expression of YY1 in lung cancer cells. Collectively, our study showed a critical role of YY1 in the regulation of tumorigenesis, partly through its downstream target PVT1	28972861	2017	Transcription Factor YY1 Modulates Lung Cancer Progression by Activating lncRNA-PVT1
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	prostate cancer	C61.9	NA	qPCR, ChIP etc.	cell lines (PC3, 1542-CP)	differential expression	The risk allele (G) of rs378854 (A>G) reduces binding of the transcription factor YY1 in vitro. The region surrounding rs378854 interacts with the MYC and PVT1 promoters.Expression of the PVT1 oncogene in normal prostate tissue increased with the presence of the risk allele of rs378854, while expression of MYC was not affetced.	21814516	2011	A functional variant at a prostate cancer predisposition locus at 8q24 is associated with PVT1 expression.
SAMMSON	LINC01212	101927152	ENSG00000240405	NR_110000	GRCh38_3: 69999550-70518064	melanoma	NA	M8720/3	qPCR, RIP etc.	cell lines (Mel501, SK-MEL-28), melanoma tissues	up-regulated	Our results indicate that silencing of the lineage addiction oncogene SAMMSON disrupts vital mitochondrial functions in a cancer-cell-specific manner; this silencing is therefore expected to deliver highly effective and tissue-restricted antimelanoma therapeutic responses.	27008969	2016	Melanoma addiction to the long non-coding RNA SAMMSON
SOX2OT	SOX2-OT, NCRNA00043, SOX2OT	347689	ENSG00000242808	NR_004053	GRCh38_3:180989762-181836880	lung squamous cell carcinoma	C34	M8070/3	qPCR etc.	LSCC tissues	up-regulated	In conclusion, eight out of the nine tested genes were recurrently over-expressed, but SOX2 and SOX2OT were the most consistently highly over-expressed and thus are the best candidates to be driver genes of 3q26.3 amplifications.	20126410	2010	SOX2 is an oncogene activated by recurrent 3q26.3 amplifications in human lung squamous cell carcinomas.
AC002519.6	NA	NA	ENSG00000261457	NA	GRCh38_16:31802947-31807973	bladder cancer	C67	NA	microarray, qPCR etc.	bladder cancer tissues	down-regulated	Five lncRNAs and four mRNAs were chose for verification of the microarray results in 30 pairs of samples by quantitative real-time PCR. qRT-PCR assay showed that the expression of lncRNA RP11-359E19.2 was upregulated, whereas AL928768.3 and AC002519.6 as well as RP11-79H23.3 and AK021804 were downregulated.	27363013	2016	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.
AGAP2-AS1	AGAP2-AS1, PUNISHER	100130776	ENSG00000255737	NR_027032	GRCh38_12:57726271-57728356	gastric cancer	C16	NA	qPCR, RNAi, Western blot, RIP, ChIP, Luciferase reporter assay, Cell proliferation assay, Cell migration and invasion assay etc.	gastric cancer tissues, cell lines (BGC823, SGC7901, AGS, MGC803, and MKN45)	up-regulated	AGAP2-AS1 was highly expressed in the GC tissues and cell lines. Knockdown of AGAP2-AS1 significantly inhibited GC cell proliferation, migration, and invasion in vitro and tumor growth in vivo. AGAP2-AS1 overexpression promoted cell growth and invasion. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.	28209205	2017	Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.
AK021804	NA	NA	NA	NA	GRCh38_11:122096198-122097680	bladder cancer	C67	NA	microarray, qPCR etc.	bladder cancer tissues	down-regulated	Five lncRNAs and four mRNAs were chose for verification of the microarray results in 30 pairs of samples by quantitative real-time PCR. qRT-PCR assay showed that the expression of lncRNA RP11-359E19.2 was upregulated, whereas AL928768.3 and AC002519.6 as well as RP11-79H23.3 and AK021804 were downregulated.	27363013	2016	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.
AL928768.3	AL928768.3	NA	NA	NA	NA	bladder cancer	C67	NA	microarray, qPCR etc.	bladder cancer tissues	down-regulated	Five lncRNAs and four mRNAs were chose for verification of the microarray results in 30 pairs of samples by quantitative real-time PCR. qRT-PCR assay showed that the expression of lncRNA RP11-359E19.2 was upregulated, whereas AL928768.3 and AC002519.6 as well as RP11-79H23.3 and AK021804 were downregulated.	27363013	2016	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.
CRNDE	CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5	NA	ENSG00000245694	NA	GRCh38_16:54845189-54929189	colorectal cancer	C19.9	NA	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell migration and invasion assay etc.	CRC tissues, cell lines (SW480, HCT116 and HT-29)	up-regulated	We confirmed the upregulation of CRNDE in both primary specimens from colorectal cancer patients and colorectal cancer cell lines. Overexpression of CRNDE promoted the migration and invasion potency of colorectal cancer cells. Knockdown of CRNDE with OXA treatment decreased cell viability and promoted DNA damage and cell apoptosis. Further in-depth mechanistic studies revealed that CRNDE functioned as a competing endogenous RNA for miR-136, led to the de-repression of its endogenous target, E2F transcription factor 1 (E2F1).	28115855	2017	Long noncoding RNA CRNDE functions as a competing endogenous RNA to promote metastasis and oxaliplatin resistance by sponging miR-136 in colorectal cancer.
ENST00000460164	NA	NA	NA	NA	NA	triple negative breast cancer	C50	NA	microarray, qPCR etc.	triple-negative breast cancer tissues	up-regulated	We found that the expression levels of TCONS_l2_00003938, ENST00000460164, ENST00000425295, MALAT1 and HOTAIR were significantly higher in tumor tissues than non-tumor tissues, whereas there were no significant differences in the expression levels of the other 3 lncRNAs. Our study identified a set of lncRNAs that were consistently aberrantly expressed in TNBC, and these dysregulated lncRNAs may be involved in the development and/or progression of TNBC.	25996380	2015	Microarray Expression Profiling of Dysregulated Long Non-Coding RNAs in Triple-Negative Breast Cancer.
GAPLINC	GAPLINC, LINC01540	100505592	ENSG00000266835	NR_110429	GRCh38_18:3466250-3478978	gastric cancer	C16	NA	microarray, ISH etc.	gastric cancer tissues	up-regulated	GAPLINC is a 924-bp-long lncRNA that is highly expressed in gastric cancer tissues. GAPLINC suppression and with gene expression profiling in gastric cancer cells revealed alterations in cell migration pathways, with CD44 expression the most highly correlated. Manipulating GAPLINC expression altered CD44 mRNA abundance and the effetcs of GAPLINC on cell migration and proliferation were neutralized by suppressing CD44 expression.	25277524	2014	Long Noncoding RNA GAPLINC Regulates CD44-Dependent Cell Invasiveness and Associates with Poor Prognosis of Gastric Cancer.
GAPLINC	GAPLINC, LINC01540	100505592	ENSG00000266835	NR_110429	GRCh38_18:3466250-3478978	gastric cancer	C16	NA	qPCR, RNAi, Western blot, RIP, ChIP, Luciferase reporter assay etc.	gastric cancer tissues, cell lines (GEF-1, HFE-145, MKN45, SGC7901, HEK-293T)	up-regulated	GAPLINC was overexpressed in GC tissues and promoted tumor migration and invasive behavior. GAPLINC overexpression was associated with poor prognosis in GC patients. Luciferase reporter assays and chromatin immunoprecipitation assays confirmed that HIF-1a binds to the promoter region of GAPLINC and activates its transcription. GAPLINC knockdown inhibited hypoxia-induced tumor proliferation in vivo.	27729869	2016	Hypoxia Promotes Gastric Cancer Malignancy Partly through the HIF-1a Dependent Transcriptional Activation of the Long Non-coding RNA GAPLINC.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	colorectal cancer	C19.9	NA	microarray, qPCR, RIP, ChIP etc.	cell lines (DLD1, HCT116, HT29 and SW480)	differential expression	H19 silencing blocked G1-S transition, reduced cell proliferation, and inhibited cell migration. Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. We further demonstrated that reduced CDK8 expression underlies changes of B-catenin activity, and identified that H19 interacts with macroH2A, an essential regulator of CDK8 gene transcription.	27789274	2016	H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-B-Catenin Signaling in Colorectal Cancer.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	breast cancer	C50	NA	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown	breast cancer cell lines (MDA-MB-231,MCF-7, SK-BR-3 and HEK293T)	up-regulated	Furthermore, H19 knockdown decreases PDK1 xpression in hypoxia, and ablation of PDK1 counteracts H19-mediated glycolysis and self-renewal ability in vitro and in vivo.Reprogramming is referred to as the conversion of differentiated cells to a stem-like state. Ectopic expression of four transcription factors (Oct4, Klf4, Sox2 and c-Myc) reprograms various types of somatic cells to induced pluripotent stem cells. Accordingly, H19 and PDK1 expression exhibits strong correlations in primary breast carcinomas. H19 acting as a competitive endogenous RNA sequesters miRNA let-7 to release Hypoxia-inducible factor 1a, leading to an increase in PDK1 expression. Lastly, aspirin markedly attenuates glycolysis and cancer stem-like characteristics by suppressing both H19 and PDK1. 	29106390	2017	Glycolysis gatekeeper PDK1 reprograms breast cancer stem cells under hypoxia.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	gastric cancer	C16	NA	qPCR, Western blot etc.	Gastric Cancer tissues, cell lines (AGS and GES-1)	up-regulated	we found that H19 depended on miR-675 to enhance the proliferation and invasion of gastric cancer AGS cells, and the expression of miR-675 was positively correlated with H19 in patients with gastric cancer. Subsequently, the tumor-suppressor runt domain transcription factor 1 (RUNX1) was confirmed to be a downstream molecule of H19/miR-675 axis, since overexpression of H19 or miR-675 significantly decreased RUNX1 expression in AGS cells, and knockdown of H19 or miR-675 enhanced RUNX1 expression.	26931432	2016	Long Noncoding RNA H19-Derived miR-675 Enhances Proliferation and Invasion via RUNX1 in Gastric Cancer Cells
HOXD-AS1	HAGLR, HOXD-AS1, Mdgt	401022	ENSG00000224189	NR_033979	GRCh38_2:176164051-176188958	glioblastoma	NA	M9440/3	qPCR, Western blot, Luciferase reporter assay etc.	glioma tissues, cell line (HEK-293T)	up-regulated	HOXD-AS1 expression was upregulated in glioma tissues and in glioma cell lines.HOXD-AS1 overexpression promoted cell migration and invasion in vitro, whereas knockdown of HOXD-AS1 expression repressed these cellular processes. Mechanistic studies further revealed that HOXD-AS1 could compete with the transcription factor E2F8 to bind with miR-130a,thus affecting E2F8 expression. Additionally, reciprocal repression was observed between HOXD-AS1 and miR-130a,and miR-130a mediated the tumor-suppressive effects of HOXD-AS1 knockdown. 	29341117	2018	HOXD-AS1/miR-130a sponge regulates glioma development by targeting E2F8.
HULC	HULC, HCCAT1, LINC00078, NCRNA00078	728655	ENSG00000251164	NR_004855	GRCh38_6:8435568-9294133	liver cancer	C22.0	NA	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay etc.	HCC tissues, cell lines (HepG2, Huh7, HepG2.2.15 etc.)	up-regulated	Levels of HULC were positively correlated with levels of SPHK1 and its product, sphingosine-1-phosphate (S1P), in patients HCC samples. HULC increased SPHK1 in hepatoma cells. Mechanistically, HULC activated the promoter of SPHK1 in hepatoma cells through the transcription factor E2F1. Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) further showed that E2F1 was capable of binding to the E2F1 element in the SPHK1 promoter. HULC increased the expression of E2F1 in hepatoma cells and levels of HULC were positively correlated with those of E2F1 in HCC tissues. Intriguingly, HULC sequestered miR-107, which targeted E2F1 mRNA 3'UTR, by complementary base pairing. Functionally, si-SPHK1 remarkably abolished the HULC-enhanced tumor angiogenesis in vitro and in vivo.	26540633	2015	Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1).
HULC	HULC, HCCAT1, LINC00078, NCRNA00078	728655	ENSG00000251164	NR_004855	GRCh38_6:8435568-9294133	liver cancer	C22.0	NA	qPCR, Western blot, Luciferase reporter assay etc.	liver cancer tissues, cell lines (CREB, HULC, Prkacb etc.)	up-regulated	The study elucidates that fine tuning of HULC expression is part of an auto-regulatory loop in which it's inhibitory to expression and activity of miR-372 allows lncRNA up-regulated expression in liver cancer.	20423907	2010	CREB up-regulates long non-coding RNA, HULC expression through interaction with microRNA-372 in liver cancer.
LINC00174	NA	285908	ENSG00000179406	NR_026873	GRCh38_7:66376044-66493566	colorectal cancer	C19.9	NA	qPCR, Luciferase reporter assay etc.	lung tissues, cell lines (DLD1, HCT116, LOVO, RKO, LS174T, HCT8, HR28348, HT29, SW620, SW480 and NCM460)	up-regulated	increased expression of LINC00174 in CRC tissues and cells in comparison to their corresponding controls.Moreover,the aberrant overexpression of LINC00174 indicated the poor prognosis of CRC patients.Silence of LINC00174 was able to repress CRC cell growth in vitro and in vivo.We first reported that transcription factor STAT1 mediated LINC00174 expression in CRC. In addition, rescue assay was performed to further confirm that LINC00174 contributed to CRC progression by regulating miR-1910-3p/TAZ signal pathway. Taken together, our study discovered the oncogenic role of LINC00174 in clinical specimens and cellular experiments,showing the potential LINC00174/miR-1910-3p/TAZ pathway.	29729381	2018	STAT1-mediated upregulation of lncRNA LINC00174 functions a ceRNA for miR-1910-3p to facilitate colorectal carcinoma progression through regulation of TAZ.
LINC00210	LINC00210, NCRNA00210	100885798	ENSG00000231814	NR_048550	GRCh38_1:217892900-217920804	non small cell lung cancer	C34	M8046/3	microarray, qPCR, RNAi, Western blot etc.	cell lines (A549, CDDP etc.)	up-regulated	For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway.	23741487	2013	The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell.
LINC01287	TCONS_l2_00027522	103724390	ENSG00000234722	NR_125776	GRCh38_7:153399920-153413963	hepatocellular carcinoma	C16	NA	qRT-PCR， Western blot assay， ChIP， Luciferase reporter assay	HCC cell lines (HepG-2, Huh7, Bel7402 and Hep3B) and the normal liver epithelial cell line LO2, HCC tissues and matched normal tissue	up-regulated	the expression of LINC01287 was increased in HCC cell lines, as well as tissues. Knockdown of LINC01287 decreased HCC cell growth and invasion both in vitro and in vivo. LINC01287 can negatively regulate miR-298 expression by acting as a ceRNA. miR-298 directly targeted STAT3 and inhibited its expression. LINC01287 exerted its function via the miR-298/STAT3 axis in HCC. Interestingly, STAT3 elevated LINC01287 expression via c-jun, which bound to the LINC01287 promoter. A feedback loop was also discovered between LINC01287 and the miR-298/STAT3 axis.	30001751	2018	LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells.
linc-ROR	LINC-ROR, ROR, lincRNA-RoR	100885779	ENSG00000258609	NR_048536	GRCh38_18:57054558-57072119	prostate cancer	C61.9	NA	qPCR, microarray etc.	cell lines (Du145, 22RV1)	down-regulated	lncRNA-ROR and Oct4 mRNA both contain miR-145 binding sites, and Oct4 and lncRNA-ROR directly compete for microRNA binding. Curcumin induced high miR-145 expression and inhibited the expression of lncRNA-ROR. The tumorigenicity of curcumin- treated HuPCaSCs in nude mice was significantly reduced. In summary, reducing the expression of endogenous lncRNA-ROR could effectively increase the available concentration of miR-145 in HuPCaSCs, where miR-145 prevents cell proliferation by decreasing Oct4 expression. In particular, we hypothesized that lncRNA-ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Oct4. Thus, curcumin suppresses the proliferation, in vitro invasion, and tumorigenicity of HuPCaSCs through ceRNA effect of miR-145 and lncRNA-ROR caused.	28843521	2017	Curcumin suppresses proliferation and in vitro invasion of human prostate cancer stem cells by ceRNA effect of miR-145 and lncRNA-ROR
linc-ROR	LINC-ROR, ROR, lincRNA-RoR	100885779	ENSG00000258609	NR_048536	GRCh38_18:57054558-57072119	pancreatic cancer	C25	NA	qPCR, RNAi, Western blot, Northern blot, Flow cytometry assay, FISH etc.	pancreatic cancer tissues	up-regulated	Compared with adjacent non-tumor tissues, ROR was up-regulated in most tumor tissues. Knockdown of ROR by RNA interference in PCSCs inhibited proliferation, induced apoptosis and decreased migration. Moreover, ROR silencing resulted in significantly decreased tumourigenicity of PCSCs in nude mice than controls. In particular, ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Nanog.	26636540	2016	ROR functions as a ceRNA to regulate Nanog expression by sponging miR-145 and predicts poor prognosis in pancreatic cancer.
linc-ROR	LINC-ROR, ROR, lincRNA-RoR	100885779	ENSG00000258609	NR_048536	GRCh38_18:57054558-57072119	gastric cancer	C16	NA	qPCR, RNAi etc.	cell lines (AGS1, MGC803, SGC7901, and MKN48), gastric adenocarcinomas tissues	down-regulated	LINCROR could sponge the miR-148a, miR-145 and miR-21 and can act as ceRNA modulating the miRNA-mediated post-transcriptional regulation of EGFR, KLF4, DNMT1 and AGO4 . The downregulation of LINCROR when its target miR-145 abundantly expressed.In addition, we observed the expression level LINCROR directly correlated with the overexpression of the miR-145. This relationship has been already reported in colon cancer and shown to be involved in overall survival. Our results suggest that reduced LINCROR/high miR-145 might be associated with better prognosis. LINCROR is an active member associated with reprogramming and stemness-related transcription factors. Downregulation of LINCROR by miR-145 might impair the cancer stemness by deregulation of another transcription factor KLF4 .	29719612	2018	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  
linc-ROR	LINC-ROR, ROR, lincRNA-RoR	100885779	ENSG00000258609	NR_048536	GRCh38_18:57054558-57072119	colon cancer	C18	NA	qPCR, Western blot, luciferase reporter assay etc.	cell lines (HB56, HB96,TSCC, Tca8113, SCC-9 and CAL27, HEK-293T), Oral cancer tissues	up-regulated	LincRNA-ROR was frequently up-regulated and inversely correlated with miR-145 down-regulation in the colon cancer specimens. The levels of CD44, CD133, Oct4, Sox2, Nanog, lincRNA-ROR in CD44(+) CD133(+) cells were significantly increased,while miR-145 was decreased compared with CD44(-)CD133(-)cells(P<0.05). The levels of CD44,CD133,lnc-ROR in CD44(+) CD133(+) cells were significantly reduced upon cell adherence, while miR-145 was significantly increased. Bioinformatics analysis revealed that lincRNA-ROR shared miRNA response elements with core transcription factors Oct4,Sox2 and Nanog. MiR-145 significantly inhibited the expression of lincRNA-ROR, Oct4, Sox2 and Nanog. Silencing lincRNA-ROR significantly inhibited colon cancer stem cells proliferation and increased the sensitivity to chemotherapy. Linc-ROR functions as a key ceRNA to prevent core TFs,e.g.Oct4, Sox2, Nanog, from miR-145-mediated suppression in colon cancer stem cells and regulates cell proliferation and chemosensitivity.	29690669	2018	LincRNA-ROR functions as a ceRNA to regulate Oct4, Sox2, and Nanog expression by sponging miR-145 and its effect on biologic characteristics of colonic cancer stem cells 
lncRNA-AF147447	AC009084.3	NA	ENSG00000280416	NA	GRCh38_16:66944660-66945096	gastric cancer	C16	NA	microarray, qPCR, Western blot, Luciferase reporter assay etc.	gastric cancer tissues, cell lines (7901 and MKN45)	down-regulated	We identified an lncRNA-AF147447 decreased expressed by H. pylori infection, which can inhibit GC proliferation and invasion in vitro and in vivo, act as a tumor suppressor in the development of H. pylori induced GC. LncRNA AF147447 could repress MUC2 expression by direct binding or increasing miR-34c expression. We also found that transcription factor E2F1 could be recruited to lncRNA AF147447 promoter by RNA immunoprecipatation and RNA pull down assays.	27835575	2016	Helicobacter pylori infection related long noncoding RNA (lncRNA) AF147447 inhibits gastric cancer proliferation and invasion by targeting MUC2 and up-regulating miR-34c.
lncRNA-TTN-AS1	NA	100506866	ENSG00000237298	NR_038272	GRCh38_2:178521183-178779963	esophageal squamous cell cancer	NA	NA	Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RNAi, RIP	ESCC tissue, ESCC cell lines (Eca-109, KYSE 30, KYSE 150, KYSE180, KYSE410, KYSE450, KYSE510, TE-10 and TE-13)	up-regulated	lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade.Moreover,lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR,which further promotes ESCC invasion cascades.	29101304	2017	Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis.
LOC554202	MIR31HG, hsa-lnc-31, LncHIFCAR	554202	ENSG00000171889	NR_027054	GRCh38_9:21455642-21559669	laryngeal squamous cell cancer	C32.3	NA	microarray, qPCR etc.	LSCC tissues	up-regulated	To further validate the results of the microarray analysis, the expression of lncRNAs and mRNAs selected above were analyzed by qRT-PCR in an independent cohort of 30 pairs of LSCC cancer tissues and adjacent non-neoplastic tissues. The results of qRT-PCR were consistent with those in microarray with the same trend.	28033431	2016	Integrated Analysis of Long Noncoding RNA and mRNA Expression Profile in Advanced Laryngeal Squamous Cell Carcinoma.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	renal cell carcinoma	C64.9	NA	qPCR, Luciferase reporter assay etc.	RCC tissues	up-regulated	We found that MALAT1 expression was higher in human RCC tissues where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed.	25600645	2015	Long noncoding RNA MALAT1 promotes aggressive renal cell carcinoma through Ezh2 and interacts with miR-205.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	glioma	NA	M9380/3	qPCR, Western blot etc.	cell lines (U87 and U251)	up-regulated	we found that the expression of lncRNA MALAT1 was significantly increased in glioma tissues compared with that of paracancerous tissues. Meanwhile, the expression of MALAT1 was highly expressed in U98 and U251 cells. In order to explore the function of MALAT1, the expression of MALAT1 was greatly reduced in U87 and U251 cells transfected with siRNA specifically targeting MALAT1. Consequently, cell viability of U87 and U251 cells were drastically decreased after the knockdown of MALAT1. Concomitantly, the apoptosis rate of the two cell lines was dramatically increased. Furthermore, the expression levels of some tumor markers were reduced after the knockdown of MALAT1, such as CCND1 and MYC	27134488	2016	Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	ovarian cancer	C56.9	NA	microarray, qPCR, in vitro knockdown etc.	cell lines (SKOV3, 293T)	up-regulated	The results showed that MALAT1 inhibition significantly suppressed tumorigenity in vitro and in vivo. Compared with the control cells, 921 genes in the MALAT1-knockdown cells were deregulated by at least two-fold.	27313681	2016	Inhibition of the long non-coding RNA MALAT1 suppresses tumorigenicity and induces apoptosis in the human ovarian cancer SKOV3 cell line.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	glioma	NA	M9380/3	qPCR, Western blot, RIP, ChIP, Luciferase reporter assay etc.	glioma tissues, cell lines (hCMEC/D3, ECs)	up-regulated	Our results proved that MALAT1 expression was up-regulated in brain microvessels of human glioma and glioma endothelial cells (GECs) which were obtained by co-culturing endothelial cells with glioma cells. Functionally, knockdown of MALAT1 resulted in an impairment and increased the permeability of BTB as well as decreased the expression of ZO-1, occludin and claudin-5 in GECs. Further, there was reciprocal repression between MALAT1 and miR-140, and miR-140 mediated the effects that MALAT1 knockdown exerted. Mechanistic investigations defined that nuclear factor YA (NFYA), a CCAAT box-binding transcription factor, was a direct and functional downstream target of miR-140, which was involved in the MALAT1 knockdown induced regulation of BTB function.	26619802	2015	Knockdown of long non-coding RNA MALAT1 increases the blood-tumor barrier permeability by up-regulating miR-140
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	gastric cancer	C16	NA	qPCR, RNAi, Western blot, ChIP etc.	gastric cancer tissues, cell lines (MKN28, SGC7901, BGC823 etc.)	up-regulated	The expression of MALAT1 was up-regulated in GC tissues and three cell lines. Si-MALAT1/pcDNA-MALAT1 induced the decrease of cell invasion and migration, while the effects were reversed by the transfection of pcDNA-EGFL7/si-EGFL7. ChIP assay showed that MALAT1 regulated EGFL7 expression by altering the level of H3 histone acetylation in EGFL7 promoter. In tumor xenotransplant mice, down-regulated MALAT1 contributed to the inhibition of tumor metastasis.	27259812	2016	Overexpressed MALAT1 promotes invasion and metastasis of gastric cancer cells via increasing EGFL7 expression.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay etc.	HCC tissues, cell lines (L-02, Bel-7402, Huh7, and HepG2)	up-regulated	The results showed a high expression of Sp1, Sp3 and MALAT1 in HCC vs. paired non-tumor liver tissues, which was associated with the AFP level. Co-silencing of Sp1 and Sp3 synergistically repressed MALAT1 expression. Sp1 binding inhibitor, mithramycin A (MIT), also inhibited MALAT1 expression in HCC cells.	26352013	2015	Sp1 cooperates with Sp3 to upregulate MALAT1 expression in human hepatocellular carcinoma.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Northern blot, ISH etc.	HCC tissues, cell line (CT26)	up-regulated	MALAT-1. The gene and homologs lack credible open reading frames, consistent with a highly conserved large noncoding RNA (ncRNA). In all nodules of procarcinogen-induced murine hepatocellular carcinomas (HCCs) and human HCCs, expression was markedly elevated compared to the uninvolved liver. Quantitative analyses indicated a 6-7-fold increased RNA level in HCCs versus uninvolved liver, advancing this as a molecule of interest. This ncRNA was overexpressed in all five non-hepatic human carcinomas analysed, consistent with a potential marker for neoplastic cells and potential participant in the molecular cell biology of neoplasia.	16878148	2007	A large noncoding RNA is a marker for murine hepatocellular carcinomas and a spectrum of human carcinomas.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	colorectal cancer	C19.9	NA	qPCR etc.	CRC and liver tissues	down-regulated	The expression levels of four lncRNAs (GAS5, H19, MEG3 and Yiya) were significantly different between liver metastases and primary tumors of stage IV CRC patients. Furthermore, the high expression levels of GAS5 and Yiya were significantly associated with future occurrence of liver metastases in early stage CRC patients. 	27391432	2016	Long non-coding RNAs: novel prognostic biomarkers for liver metastases in patients with early stage colorectal cancer
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	lung cancer	C34	NA	qPCR, RIP, ChIP, Cell migration assay etc.	cell lines (A549 and LC-2/ad)	up-regulated	The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-B (TGF-B)-induced EMT of human lung cancer cell lines. Knockdown of MEG3 inhibited TGF-B-mediated changes in cell morphology and cell motility characteristic of EMT and counteracted TGF-B-dependent changes in the expression of EMT-related genes such as CDH1, ZEB family, and the microRNA-200 family. Overexpression of MEG3 influenced the expression of these genes and enhanced the effects of TGF-B in their expressions. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression.	27852821	2017	MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines.
MIR100HG	MIR100HG, AGD1, linc-NeD125, lncRNA-N2	399959	ENSG00000255248	NR_024430	GRCh38_11:122028327-122556721	colorectal cancer	C19.9	NA	qPCR etc.	cell lines 	up-regulated	MIR100HG, miR-100 and miR-125b overexpression was also observed in cetuximab-resistant colorectal cancer and head and neck squamous cell cancer cell lines and in tumors from colorectal cancer patients that progressed on cetuximab. miR-100 and miR-125b coordinately repressed five Wnt/B-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness. Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6. These findings identify a clinically actionable, epigenetic cause of cetuximab resistance.	29035371	2017	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/B-catenin signaling
MIR155HG	MIR155HG, BIC, MIRHG2, NCRNA00172	114614	ENSG00000234883	NR_001458	GRCh38_21:25561909-25575168	diffuse large B-cell lymphoma	NA	M9680/3	qPCR, Northern blot etc.	Blood, cell lines (Ramos, JY25, CB33, U266, Jurkat, K562, HL60 etc.)	up-regulated	Relative to the control B cells, BIC RNA levels were elevated from 2- to 10-fold in DLBCL cells, with one sample showing an increase of >20-fold. 	15738415	2005	Accumulation of miR-155 and BIC RNA in human B cell lymphomas.
nc886	VTRNA2-1, CBL-3, CBL3, MIR886, MIRN886, VTRNA2, hsa-mir-886, hvg-5, nc886, svtRNA2-1a	100126299	ENSG00000270123	NR_030583	GRCh38_5:136080470-136080597	gastric cancer	C16	NA	RNA-seq, qPCR etc.	gastric cancer tissues, gastric cell lines	down-regulated	Our real-time RT-PCR data (Fig 1A) indicated that the expression level of nc886 was lower in a subpopulation of tumor tissues than in normal tissues. nc886 inhibits cell proliferation when ectopically expressed in gastric cancer cells.	25003254	2014	nc886, a non-coding RNA of anti-proliferative role, is suppressed by CpG DNA methylation in human gastric cancer.
NCK1-AS1	NA	NA	ENSG00000239213	NA	GRCh38_3:136841726-136862054	cervical cancer	C53	NA	Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown	cervical squamous cell carcinoma tissues, cervical cancer cell lines (HeLa, C33A and SiHa and CaSki) 	up-regulated	Functionally,we screened the CC-associated lncRNA NCK1-AS1 as a new candidate lncRNA and regulator which promotes development and progression in CC. qRT-PCR and RNA in situ hybridization (RISH) results showed that NCK1-AS1 was significantly up-regulated in 77.4% of the CC tissue group compared with the normal group.Interestingly,we demonstrated that transcription factor SP1 directly binds to the promoter to activate NCK1-AS1 expression in SiHa cells.In vitro and in vivo assays of silencing NCK1-AS1 significantly inhibited cell proliferation and invasion, with induction of cell arrest in S phase of the cell cycle. NCK1-AS1 functioned as a molecular sponge for miR-6857, antagonizing its ability to repress CDK1/6 protein translation.	29416014	2018	LncRNA NCK1-AS1 promotes proliferation and induces cell cycle progression by crosstalk NCK1-AS1/miR-6857/CDK1 pathway.
ncSRPK1	SRPK1, SFRSK1	NA	NA	NA	NA	renal cell carcinoma	C64.9	NA	microarray, qPCR, Western blot etc.	RCC tissues	up-regulated	Four lncRNAs mapping to intronic regions, namely ncC11orf49, ncHDAC5, ncRAB31 and ncSRPK1, showed a significant differential expression between tumor and nontumor paired samples as measured by qPCR.	24238219	2013	Expression analysis and in silico characterization of intronic long noncoding RNAs in renal cell carcinoma: emerging functional associations.
NEAT1	NEAT1, LINC00084, NCRNA00084, TncRNA, VINC	283131	ENSG00000245532	NR_028272	GRCh38_11:65422774-65445540	glioma	NA	M9380/3	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay etc.	cell lines (U87 MG, U251MG and HEK 293T)	up-regulated	NEAT1 was remarkably up-regulated in glioma endothelial cells (GECs). Knockdown of NEAT1 impaired the integrity and increased the permeability of the BTB, accompanied by downregulation of expression of the tight junction proteins ZO-1, occludin and claudin-5 in GECs. Knockdown of NEAT1 also down-regulated the expression of sex determining region Y-box protein 5 (SOX5), which was defined as a direct and functional downstream target of miR-181d-5p. SOX5 interacts with the promoter region of ZO-1, occludin and claudin-5 in GECs.	28185956	2017	Long non-coding RNA NEAT1 regulates permeability of the blood-tumor barrier via miR-181d-5p-mediated expression changes in ZO-1, occludin, and claudin-5.
NEAT1	NEAT1, LINC00084, NCRNA00084, TncRNA, VINC	283131	ENSG00000245532	NR_028272	GRCh38_11:65422774-65445540	breast cancer	C50	NA	qPCR, RNAi etc.	cell lines (MCF-7, MDA-MB-231)	down-regulated	we demonstrated that downregulating the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in breast cancer cells inhibited cell growth and induced cell apoptosis. In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis	27147820	2016	NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548
NEAT1	NEAT1, LINC00084, NCRNA00084, TncRNA, VINC	283131	ENSG00000245532	NR_028272	GRCh38_11:65422774-65445540	non small cell lung cancer	C34	M8046/3	qPCR, Western blot etc.	lung tissues, cell lines (A549, SPC-A1, H1299, 95D, SK-MES-1, NCI-H520)	up-regulated	NEAT1 was highly expressed in NSCLC,and high NEAT1 expression was associated with a shorter overall survival.NEAT1 promoted NSCLC cell growth and affected the cell cycle process in vitro. Furthermore, NEAT1 was observed to bind hsa-miR-377-3p, functioning as a competing endogenous RNA, which resulted in de-repression of its target gene E2F transcription factor 3 (E2F3). E2F3, as an oncogene, may promote NSCLC progression.These results suggested that NEAT1 may promote the development of NSCLC through the miR-377-3p-E2F3 pathway.	29085511	2017	Long non-coding RNA NEAT1 regulates E2F3 expression by competitively binding to miR-377 in non-small cell lung cancer
PCA3	PCA3, DD3, NCRNA00019, PCAT3	50652	ENSG00000225937	NR_015342	GRCh38_9:76691980-76863307	prostate cancer	C61.9	NA	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay etc.	prostate cancer tissues, cell lines (RWPE-1, LNCaP)	differential expression	In the present study, the level of PCA3 expression in prostate cancer cells was reduced by small interfering RNA (siRNA). Subsequently, the ability of LNCaP cell proliferation, invasion, and migration of PCa was compromised both in vivo and in vitro with the occurrence of cell autophagy. The transcription factor, Snail, activated the expression of lncRNA PCA3, which could inhibit the translation of PRKD3 protein via competitive miR-1261 sponging, and thus high expression of PRKD3 further promoted invasion and migration of prostate cancer.	27743381	2016	Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells.
PlncRNA-1	CBR3-AS1, PlncRNA-1, PlncRNA1	100506428	ENSG00000236830	NR_038892	GRCh38_21:36131767-36175815	prostate cancer	C61.9	NA	qPCR, Western blot, Northern blot, RIP, ChIP, Flow cytometry assay etc.	prostate cancer tissues, cell lines (22RV1, LNCaP, PC3, DU145)	up-regulated	In this study, we demonstrated that long non-coding RNA PlncRNA-1, whose expression is promoted by Androgen Receptor (AR), protects AR from microRNA-mediated suppression in PCa cells. PlncRNA-1 knockdown resulted in the up-regulation of a series of AR-targeting microRNAs, among which miR-34c and miR-297 were found to regulate both AR and PlncRNA-1 expression at the post-transcriptional level. Together, the data generated in this study indicate that PlncRNA-1 sponges AR-targeting microRNAs to protect AR from microRNA-mediated down-regulation and that these events form a regulatory feed-forward loop in the development of PCa.	26808578	2016	A feed-forward regulatory loop between androgen receptor and PlncRNA-1 promotes prostate cancer progression.
PTAF	NA	NA	NA	NA	NA	ovarian cancer	C56.9	NA	qPCR, Western blot, etc.	ovarian cancer tissues, cell lines (SKOV3, A2780, OVCAR-3)	up-regulated	we provided evidence that the lncRNA PTAF-miR-25-SNAI2 axis controlled EMT in OvCa. Our results revealed that up-regulated PTAF induced elevated SNAI2 expression by competitively binding to miR-25, which in turn promoted OvCa cell EMT and invasion.The mesenchymal OvCa patients in the TCGA dataset with high PTAF expression showed a poorer prognosis than those with low PTAF expression.  we found that miR-25 not only had binding sites within SNAI2, a key TF regulating EMT, and PTAF but also had an inverse expression relationship with both SNAI2 and PTAF. 	29929545	2018	Systematic analyses reveal long non-coding RNA (PTAF)-mediated promotion of EMT and invasion-metastasis in serous ovarian cancer.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	prostate cancer	C61.9	NA	RNA-seq, qPCR, Western blot etc.	prostate cancer tissues, cells lines (PC-3, DU145, 22RV1 and WPMY)	up-regulated	PVT1 promotes prostate cancer invasion and metastasis by modulating EMT.Furthermore,PVT1 can promote EMT by up-regulation of Twist1,a transcription factor associated with EMT.We then confirmed that PVT1 acts as a sponge for miRNA-186-5p and positively regulates Twist1 by a sponge effect.Therefore, this study has revealed a novel MECHANISM for the promotion of EMT in prostate cancer by PVT1.Our findings suggest that the PVT1/miR-186/Twist1 regulatory axis may be a new therapeutic target for prostate cancer. PVT1 can reduce the expression of miR-186 as ceRNA in PCa cell lines and promotes Twist1 expression by suppressing miR-186.	29452232	2018	Long noncoding RNA PVT1 promotes EMT via mediating microRNA-186 targeting of Twist1 in prostate cancer.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	colorectal cancer	C19.9	NA	qPCR, Western blot etc.	cell line (FHC,SW480, SW620, HT29, HCT116), colorectal cancer tissues	up-regulated	PVT1 regulated the growth of CRC tumors by acting as a competing endogenous RNAs (ceRNA) and negatively regulated miR-455. Furthermore, we discovered that RUNX2,a functional transcription factor in CRC,up-regulated PVT1 expression. 	29637007	2018	A feedback loop consisting of RUNX2/LncRNA-PVT1/miR-455 is involved in the progression of colorectal cancer.    
RP11-359E19.2	RP11-359E19.2	NA	NA	NA	GRCh38_8:40114651-40127468	bladder cancer	C67	NA	microarray, qPCR etc.	bladder cancer tissues	up-regulated	Five lncRNAs and four mRNAs were chose for verification of the microarray results in 30 pairs of samples by quantitative real-time PCR. qRT-PCR assay showed that the expression of lncRNA RP11-359E19.2 was upregulated, whereas AL928768.3 and AC002519.6 as well as RP11-79H23.3 and AK021804 were downregulated.	27363013	2016	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.
RP11-79H23.3	RP11-79H23.3	NA	NA	NA	GRCh38_8:78837529-78840522	bladder cancer	C67	NA	microarray, qPCR etc.	bladder cancer tissues	down-regulated	Five lncRNAs and four mRNAs were chose for verification of the microarray results in 30 pairs of samples by quantitative real-time PCR. qRT-PCR assay showed that the expression of lncRNA RP11-359E19.2 was upregulated, whereas AL928768.3 and AC002519.6 as well as RP11-79H23.3 and AK021804 were downregulated.	27363013	2016	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.
RSU1P2	RSU1P2	NA	ENSG00000232554	NA	GRCh38_10:45099487-45154596	cervical cancer	C53	NA	qPCR, Western blot, Flow cytometry assay, Cell migration and invasion assay etc.	cervical cancer tissues, cell lines (SMMC-7721 and HepG3)	up-regulated	Here, we found that the lncRNA RSU1P2 is upregulateded in cervical cancer tissues and has a tumour-promoting role. We revealed that RSU1P2 acts as a ceRNA through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. The transcription factor N-myc forms a positive feedback loop with RSU1P2 by in turn activating its expression, thereby enhancing its oncogenic capacity.	27487126	2016	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.
SNHG14	NA	104472715	ENSG00000224078	NR_146177	GRCh38_15:24978583-25419462	clear cell renal cell carcinoma	C64.9	M8005/0	qPCR, Luciferase reporter assay, Western blot, RIP	cell lines (A-498, 786-O,Caki-2, Caki-1, HK-2)	up-regulated	SNHG14 was significantly up-regulated in ccRCC cell lines.the transcription factor SP1 can bind to the promoter region of SNHG14, resulting in the overexpression of SNHG14 in ccRCC. enhanced expression of lncRNA SNHG14 promoted cell migration and invasion through promoting N-WASP protein level. SNHG14 functioned as ceRNA to regulate N-WASP expression and cell motility ability via a miR-203-dependent manner.SNHG14 is a critical lncRNA that promotes ccRCC migration and invasion via sponging miR-203 and elevating N-WASP. 	29312804	2017	SP1-induced up-regulation of lncRNA SNHG14 as a ceRNA promotes migration and invasion of clear cell renal cell carcinoma by regulating N-WASP.
SNHG15	SNHG15, C7orf40, Linc-Myo1g, MYO1GUT	285958	ENSG00000232956	NR_003697	GRCh38_7:44983023-44986961	renal cell carcinoma	C64.9	NA	qPCR, Western blot etc.	cell lines (ACHN, OSRC2, 786O, 769P, CAKI1 and HK2)	up-regulated	In the present study, the expression levels of small nucleolar RNA host gene 15 (SNHG15) were significantly upregulated in renal cell carcinoma (RCC) tissues and cell lines compared with in adjacent tissues and a proximal tubule epithelial cell line, as determined by reverse transcription quantitative polymerase chain reaction. Subsequently, knockdown of SNHG15 expression with small interfering RNA inhibited RCC proliferation, invasion and migration, was determined by western blotting and Transwell assays. Furthermore, the present study suggested that SNHG15 may be involved in the nuclear factor-kB signaling pathway, induce the epithelial mesenchymal transition process, and promote RCC invasion and migration. SNHG16 exerts its effects by acting as a ceRNA, competitively binding miR-98 with E2F transcription factor 5 protein.	29750422	2018	Knockdown of SNHG15 suppresses renal cell carcinoma proliferation and EMT by regulating the NF-kB signaling pathway.
SNHG16	SNHG16, Nbla10727, Nbla12061, ncRAN	100507246	ENSG00000163597	NR_038108	GRCh38_17:76557766-76565348	breast cancer	C50	NA	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc.	breast cancer tissues, cell lines (MDA-MB-231, MCF-7, MDA-MB-468 and HEK293T)	up-regulated	Expression levels of SNHG16 were found to be frequently higher in breast cancer tissues than in the paired noncancerous tissues.Gain- and loss-of-function studies proved that SNHG16 significantly promoted breast cancer cell migration. In addition, we identified a positive correlation between SNHG16 and E2F5 in breast cancer tissues. Furthermore,we demonstrated that forced expression of miR-98 could partially abrogate SNHG16-mediated increase of breast cancer cells migration,suggesting that SNHG16 promoted cell migration in a miR-98 dependent manner.	28232182	2017	SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5.
UCA1	UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36	652995	ENSG00000214049	NR_015379	GRCh38_19:15828206-15836326	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc.	HCC tissues, cell lines (MHCC97L, Huh7, MHCC97H and SK-hep1)	up-regulated	UCA1 was markedly upregulated in HCC tissues. Furthermore, gain-of-function and loss-of-function analysis showed that UCA1 knockdown inhibited HCC cells proliferation and invasion in vitro and xenograft tumour growth in vivo. Moreover, UCA1 overexpression promoted cell epithelial-mesenchymal transition (EMT) in HCC via effectively sponging to miR-203 and thereby activating the expression of transcription factor Snail2.	28271214	2017	Long non-coding RNA UCA1 regulates the expression of Snail2 by miR-203 to promote hepatocellular carcinoma progression.
UCA1	UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36	652995	ENSG00000214049	NR_015379	GRCh38_19:15828206-15836326	bladder cancer	C67	NA	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	bladder cancer tissues, cell lines (5637 and UMUC-2)	differential expression	In the present study, knockdown of UCA1 decreased chemosensitivity to cisplatin/gemcitabine by suppressing cell proliferation and inducing apoptosis, while overexpression of UCA1 increased chemosensitivity in bladder cancer cells. Moreover, UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27Kip1.	27591936	2016	Long non-coding RNA UCA1 promotes cisplatin/gemcitabine resistance through CREB modulating miR-196a-5p in bladder cancer cells.
UCA1	UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36	652995	ENSG00000214049	NR_015379	GRCh38_19:15828206-15836326	colorectal cancer	C19.9	NA	qPCR, Western blot, RNAI, etc.	cell lines (SW480, NF)	up-regulated	Our results revealed that CAFs could induce upregulation of UCA1, leading to upregulation of mTOR. Up-regulation of UCA1/mTOR axis suppressed p27 and miR-143 while the expression of Cyclin-D1 and KRAS were significantly increased compared with control. Results verified that CAFs induce the EMTTFs and consequently E-cadherin was remarkably down-regulated	29948578	2018	Cancer-associated fibroblasts enhance cell proliferation and metastasis of colorectal cancer SW480 cells by provoking long noncoding RNA UCA1.
XIST	XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66	7503	ENSG00000229807	NR_001564	GRCh38_X:73820651-73852753	glioma	NA	M9380/3	qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay, Cell migration assay etc.	cell lines (hCMEC/D3, U87MG, U118MG, HEK293T)	up-regulated	lncRNA X-inactive-specific transcript (XIST) was upregulated in endothelial cells that were obtained in a BTB model in vitro. XIST knockdown increased BTB permeability and inhibited glioma angiogenesis. The analysis of the mechanism of action revealed that the reduction of XIST inhibited the expression of the transcription factor forkhead box C1 (FOXC1) and zonula occludens 2 (ZO-2) by upregulating miR-137. FOXC1 decreased BTB permeability by increasing the promoter activity and expression of ZO-1 and occludin, and promoted glioma angiogenesis by increasing the promoter activity and expression of chemokine (C-X-C motif) receptor 7b (CXCR7).	28287613	2017	Knockdown of long non-coding RNA XIST increases blood-tumor barrier permeability and inhibits glioma angiogenesis by targeting miR-137.
ZFAS1	ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1	441951	ENSG00000177410	NR_003604	GRCh38_20:49278178-49295738	epithelial ovarian cancer	C56.9	NA	qPCR, Cell transfection, Western blot, Luciferase reporter assay, MTT assay etc.	EOC tissues, cell lines (OVCAR3, Caov3, OVCA429, SKOV3, A2780, and COV644)	up-regulated	ZFAS1 was upregulated in epithelial ovarian cancer tissues, and was negatively correlated to the overall survival rate of patients.While depletion of ZFAS1 inhibited proliferation, migration, and development of chemoresistance, overexpression of ZFAS1 exhibited an even higher proliferation rate, migration activity, and chemoresistance in EOC cell lines. We further found miR-150-5p was a potential target of ZFAS1, which was downregulated in epithelial ovarian cancer tissue.MiR-150-5p subsequently inhibited expression of transcription factor Sp1, as evidence by luciferase assays. Inhibition of miR-150-5p rescued the suppressed proliferation and migration induced by depletion of ZFAS1 in epithelial ovarian cancer cells,at least in part. 	28099946	2017	Long non-coding RNA ZFAS1 interacts with miR-150-5p to regulate Sp1 expression and ovarian cancer cell malignancy.
AFAP1-AS1	AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740	84740	ENSG00000272620	NR_026892	GRCh38_4:7754090-7778928	gallbladder cancer	C23.9	NA	qPCR, RNAi, Western blot etc.	GBC tissues, cell lines (NOZ, H69 ,GBC-SD and SGC-996)	up-regulated	The expression levels of lncRNA AFAP1-AS1 were significantly elevated in GBC tissues and GBC cell lines. In addition, the expression level of lncRNA AFAP1-AS1 was significantly associated with tumor sizes and the higher expression of lncRNA AFAP1-AS1 was correlated with poor prognosis in GBC patients. Knockdown of LncRNA AFAP1-AS1 suppressed cell growth and invasion in NOZ and GBC-SD cells. Furthermore, we found that knockdown of LncRNA AFAP1-AS1 in GBC cells inhibited EMT by down-regulating the transcription factor Twist1 and Vimentin and up-regulated the E-cadherin.	27810781	2016	Overexpression of LncRNA AFAP1-AS1 predicts poor prognosis and promotes cells proliferation and invasion in gallbladder cancer.
AK023391	NA	NA	NA	NA	GRCh_8:123500153-123501863	gastric cancer	C16	NA	qPCR, microarray, western blot	gastric cancer tissues, cell lines(HGC-27, AGS, SGC-7901,BGC-823, and MGC-803,GES-1)	up-regulated	Expression of lncRNA AK023391 was significantly upregulated in gastric cancer samples and cell lines in comparison to adjacent normal tissues, and was positively correlated with poor survival in patients with gastric cancer.AK023391 expression acted as an independent prognostic factor for survival in patients with gastric cancer. Knockdown of AK023391 inhibited cell growth and invasion both in vitro and in vivo, and induced apoptosis and cell cycle arrest in gastric cancer cells,whereas its overexpression reversed these effects. PI3K/Akt signaling mediated the NF-kB, FOXO3a, and p53 pathways. Moreover,downstream transcription factors, such as c-myb, cyclinB1/G2, and BCL-6 might be involved in AK023391-induced tumorigenesis in gastric cancer.	29282102	2017	LncRNA AK023391 promotes tumorigenesis and invasion of gastric cancer through activation of the PI3K/Akt signaling pathway.
AK055347	FAM78B	149297	ENSG00000188859	NA	GRCh38_1:166057426-166166969	osteosarcoma	NA	M9180/3	qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc.	osteosarcoma tissues, cell lines (SOSP-9607, MG63 and F5M2)	differential expression	Notably, downregulation of Oct4 decreased the expression of AK055347, a newly identified long noncoding RNA (lncRNA) in human tissues. The downregulation of AK055347 by siRNA resulted in a significant suppressive effect on proliferative and invasive ability, and promotion of cell apoptosis in osteosarcoma cells.	28123573	2017	Transcription factor Oct4 promotes osteosarcoma by regulating lncRNA AK055347.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	renal cell carcinoma	C64.9	NA	qPCR, RNAi, Western blot, Cell migration and invasion assay, CCK-8 assay etc.	RCC tissues, cell lines (786-O, A498, caki-1 and caki-2, and HEK-293T)	up-regulated	ANRIL was highly expressed in RCC tissues and RCC cell lines. ANRIL significantly promoted cell proliferation, migration, invasion and EMT but inhibited cell apoptosis. Additionally, the expression levels of B-catenin, Ki-67, glycogen synthase kinase 3B (GSK-3B), phosphorylated GSK-3B, T cell transcription factor 4 (TCF-4) and leukemia enhancer factor 1 (LEF-1) were all markedly up-regulated by ANRIL.	28251886	2017	Highly Expressed Antisense Non-coding RNA in the INK4 Locus Promotes 5 Growth and Invasion of Renal Clear Carcinoma Cells Via the B-catenin Pathway.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	nasopharyngeal cancer	C11	NA	RT-qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP	NPC cell lines (C666-1, SUNE-1, CNE1, CNE2 and HNE-1)	up-regulated	Mechanistically, SOX2 binds with ANRIL and increases its RNA level, which upregulates B-catenin signalling, resulting in enhanced nasopharyngealcarcinoma tumourigenesis. Expression levels of ANRIL are positively correlated with SOX2 and B-catenin in clinical nasopharyngeal carcinoma samples.The transcription factor SOX2 is widely recognized for its pivotal roles during mammalian embryogenesis.	29463902	2018	Upregulation of SOX2-activated lncRNA ANRIL promotes nasopharyngeal carcinoma cell growth.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, RIP etc.	HCC tissues, cell lines (HepG2, Hep3B, MHCC-97H)	up-regulated	ANRIL expression was up-regulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. Moreover, taking advantage of loss of function experiments in HCC cells, we found that knockdown of ANRIL expression could impair cell proliferation and invasion and induce cell apoptosis both in vitro and in vivo.	25966845	2015	Long non-coding RNA ANRIL is up-regulated in hepatocellular carcinoma and promotes cell apoptosis by epigenetically silencing of KLF2.
ANRIL	CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS	100048912	ENSG00000240498	NR_003529	GRCh38_9:21994778-22121097	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, RIP, ChIP, Flow cytometry assay, Cell proliferation assay etc.	HCC tissues, cell lines (HepG2, Hep3B, MHCC-97H)	up-regulated	ANRIL expression was up-regulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. Moreover, taking advantage of loss of function experiments in HCC cells, we found that knockdown of ANRIL expression could impair cell proliferation and invasion and induce cell apoptosis both in vitro and in vivo.	27391317	2015	Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell proliferation by epigenetic silencing of KLF2.
CASC15	CASC15, LINC00340, lnc-SOX4-1	401237	ENSG00000272168	NR_015410	GRCh38_6:21664772-22368328	B-acute lymphoblastic leukemia	NA	M9826/3	qPCR, Luciferase assay, RIP etc.	B-ALL and AML patients tissues, cell lines (RS4;11, MV4;11, REH, 697, Nalm-6, and 70Z/3 and the HEK 293 T cell line)	up-regulated	CASC15 is a conserved lncRNA that was upregulated in pediatric B-acute lymphoblastic leukemia (B-ALL) with t (12; 21) as well as pediatric acute myeloid leukemia (AML) with t (8; 21), both of which are associated with relatively better prognosis. CASC15 regulated cellular survival, proliferation, and the expression of its chromosomally adjacent gene, SOX4. Differentially regulated genes following CASC15 knockdown were enriched for predicted transcriptional targets of the Yin and Yang-1 (YY1) transcription factor. Interestingly, we found that CASC15 enhances YY1-mediated regulation of the SOX4 promoter. CASC15 in RUNX1-translocated leukemia, and point towards a mechanistic basis for its action. CASC15 expression was not statistically associated with survival by Kaplan-Meier analysis or in a multivariate regression model 	28724437	2017	The lncRNA CASC15 regulates SOX4 expression in RUNX1-rearranged acute leukemia.
CCAT2	CCAT2, LINC00873, NCCP1	101805488	ENSG00000280997	NR_109834	GRCh38_8:127400399-127402150	ovarian cancer	C56.9	NA	qPCR, Western blot, Luciferase reporter assay, in vitro knockdown	EOC cell lines (SKOV3, A2780,HO8910, HOSE HUM-CELL-0088) 	up-regulated	Functional assays demonstrated that the knockdown of CCAT2 inhibited migration and invasion of EOC cells in vitro. Moreover, our results showed that silencing CCAT2 inhibited EMT by the upregulation of epithelial cadherin and downregulation of neural cadherin, zinc finger protein SNAI and Twist-related protein 1 in SKOV3 and A2780 cell lines.knockdown of CCAT2 inhibited the expression of  B -catenin and the activity of T-cell factor/lymphoid enhancer factor, acting as a key transcription factor of Wnt signaling pathway. Collectively, these results indicate that CCAT2 may promote EMT, at least partly through Wnt/ B -catenin signaling pathway in EOC cells.	29435081	2017	Long non-coding RNA CCAT2 promotes epithelial-mesenchymal transition involving Wnt/B-catenin pathway in epithelial ovarian carcinoma cells.
CCAT2	CCAT2, LINC00873, NCCP1	101805488	ENSG00000280997	NR_109834	GRCh38_8:127400399-127402150	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Cell migration and invasion assay etc.	HCC tissues, cell lines (HepG2, SMMC772, MHCC97H and MIHA)	up-regulated	CCAT2 was upregulated in HCC cell lines and cancerous tissues. The level of CCAT2 was positively associated with tumor-node-metastasis stages and vessel invasion. Moreover, we also found that knockdown of CCAT2 expression reduced cell migration and invasion in vitro. We further demonstrated that CCAT2 played a key role in enhancing the epithelial-mesenchymal transition (EMT) through the regulation of vimentin, E-cadherin and transcription factor snail2 expression.	28280353	2017	Long non-coding RNA CCAT2 is associated with poor prognosis in hepatocellular carcinoma and promotes tumor metastasis by regulating Snail2-mediated epithelial-mesenchymal transition.
ECONEXIN	NA	NA	NA	NA	NA	glioma	NA	M9380/3	Western blot, Microarray, luciferase reporter assay.	glioma tissue, glioma cell lines (U87,U251)	up-regulated	Our data demonstrated that ECONEXIN is a potential oncogene that regulates TOP2A by sponging miR-411-5p in glioma. In addition, our investigative approaches to identify conserved lncRNA and their molecular characterization by validation in mouse tumor models may be useful to functionally annotate novel lncRNAs, especially cancer-associated lncRNAs.which coordinately promotes self-renewal by sponging miR-145 in the cytoplasm and recruiting polycomb to repress differentiation genes by the locus-specific methylation of histone H3K27 in the nucleus.promoter region (~500 bp upstream of transcriptional start site). Transcriptional factor binding motif analysis using the JASPAR database revealed that 140 transcription factors may bind to the ECONEXIN and C130071C03Rik promoter regions.28 	28368417	2017	Oncogenic effects of evolutionarily conserved noncoding RNA ECONEXIN on gliomagenesis.
ENST00000464359	LINC00635	151658	ENSG00000241469	NR_015414	GRCh38_3:107841303-107878068	lung adenocarcinoma	C34	M8140/3	microarray, qPCR etc.	cell lines (HCC827 and HCC827-8-1)	up-regulated	To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance.	27108960	2016	Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray.
ENST00000480669	RP11-641D5.2, LOC105374205	NA	NA	NA	GRCh38_3:169447867-169477052	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	down-regulated	Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results.	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
ENST00000503938	LINC01096	NA	ENSG00000246095	NA	GRCh38_4:13546075-13546964	triple negative breast cancer	C50	NA	microarray, qPCR etc.	TNBC tissues	down-regulated	The results demonstrated that lncRNAs NONHSAT125629 and ENST00000503938 were upregulated and that XR_250621.1 and NONHSAT012762 were down-regulated in the tumor samples compared with NT samples. These qPCR results are consistent with the microarray data.	26078338	2015	Identification of novel long non-coding RNAs in triple-negative breast cancer.
ENST00000507437	RNPS1P1	NA	ENSG00000250896	NA	GRCh38_4:11371975-11372892	non small cell lung cancer	C34	M8046/3	microarray, qPCR, Cell proliferation assay etc.	cell lines (PC9, H1975, H1299 and A549)	up-regulated	Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR.	25482516	2015	Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer.
ENST00000508827	RP11-47I22.2, LOC101927780	NA	NA	NA	GRCh38_14:61556320-61570653	non small cell lung cancer	C34	M8046/3	microarray, qPCR, Cell proliferation assay etc.	cell lines (PC9, H1975, H1299 and A549)	up-regulated	Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR.	25482516	2015	Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer.
ENST00000539535	NA	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	up-regulated	Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results.	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
ERIC	ERICD, ERIC, LINC01130, TCONS_00014875	104355217	ENSG00000280303	NA	GRCh38_8:140636281-140638283	osteosarcoma	NA	M9180/3	RNA-seq, qPCR, RNAi, Western blot, ChIP etc.	cell lines (U2OS and SAOS-2)	up-regulated	We show that expression levels of ERIC were elevated upon activation of exogenous E2F1, E2F3 or endogenous E2Fs. Moreover, knockdown of either E2F1 or E2F3 reduced ERIC levels and endogenous E2F1 binds ERIC's promoter. Expression of ERIC was cell cycle regulated and peaked in G1 in an E2F1-dependent manner. Inhibition of ERIC expression increased E2F1-mediated apoptosis, suggesting that E2F1 and ERIC constitute a negative feedback loop that modulates E2F1 activity. Furthermore, ERIC levels were increased following DNA damage by the chemotherapeutic drug Etoposide, and inhibition of ERIC expression enhanced Etoposide -induced apoptosis.	24168400	2013	The long non-coding RNA ERIC is regulated by E2F and modulates the cellular response to DNA damage.
EVI1	MECOM, AML1-EVI-1, EVI1, KMT8E, MDS1, MDS1-EVI1, PRDM3, RUSAT2	2122	ENSG00000085276	NA	GRCh38_3:169083499-169663618	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Western blot, Luciferase reporter assay etc.	HCC tissues	up-regulated	Our findings suggest that EVI1 is frequently up-regulated and regulates a cluster of lncRNAs in HBV-related hepatocellular carcinoma (HCC). These findings highlight a novel mechanism for HBx-induced hepatocarcinogenesis through transcription factor EVI1 and its target lncRNAs, and provide a potential new approach to predict the functions of lncRNAs	26967394	2016	EVI1 promotes cell proliferation in HBx-induced hepatocarcinogenesis as a critical transcription factor regulating lncRNAs
EWSAT1	EWSAT1, LINC00277, NCRNA00277, TMEM84	283673	ENSG00000212766	NR_026949	GRCh38_15:69072926-69095820	Ewing sarcoma	NA	M9260/3	microarray, qPCR, Western blot, RIP etc.	cell lines (pMPCs, PSS090 and TC71)	up-regulated	Expression of EWS-FLI1 and EWSAT1 repressed gene expression, and a substantial fraction of targets that were repressed by EWS-FLI1 were also repressed by EWSAT1. Analysis of RNAseq data from primary human Ewing sarcoma further supported a role for EWSAT1 in mediating gene repression. We identified heterogeneous nuclear ribonucleoprotein (HNRNPK) as an RNA-binding protein that interacts with EWSAT1 and found a marked overlap in HNRNPK-repressed genes and those repressed by EWS-FLI1 and EWSAT1, suggesting that HNRNPK participates in EWSAT1-mediated gene repression.	25401475	2014	Long noncoding RNA EWSAT1-mediated gene repression facilitates Ewing sarcoma oncogenesis
FAL1	FALEC, FAL1, LINC00568, ncRNA-a1	100874054	ENSG00000228126	NR_051960	GRCh38_1:150515757-150518032	papillary thyroid cancer	NA	M8260/3	qPCR, Western blot etc.	cell lines (BCPAP, 8505C, C643, HTH63, and SW1736)	up-regulated	FAL1 expression was significantly higher in PTC than in paired normal thyroid tissues. 	26825907	2016	Relationship of Focally Amplified Long Noncoding on Chromosome 1 (FAL1) lncRNA with E2F Transcription Factors in Thyroid Cancer.
FENDRR	FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21	400550	ENSG00000268388	NR_033925	GRCh38_16:86474529-86509099	osteosarcoma	NA	M9180/3	qPCR, Western blot	human osteosarcoma cell lines (SaoS2, HOS, KH-OS, MG63,143B,U2-OS), OS tissues	up-regulated	Thus, we concluded that FOXF1-AS1 may promote migration and invasion of OS cells through the FOXF1/MMP-2/-9 pathway. Taken together, these findings demonstrated the underlying mechanism of FOXF1-AS1 in the regulation of OS progression and provide a novel potential target in the OS therapy.OS patients with lower expression of FOXF1 had longer overall survival time than those with higher expression. *P < 0.05, **P < 0.01.LncRNA FOXF1-AS1 is one of antisense long noncoding RNAs and its conjugate gene FOXF1 (forkhead transcription factor 1) belongs to the 43 members of transcription factor FOX gene family 31.we speculated the cytoplasmic lncRNA FOXF1-AS1 may regulate the expression of FOXF1 and MMPs at the posttranscriptional level as an endogenous competing RNA to sponge the related miRNAs.	29104509	2017	Antisense lncRNA FOXF1-AS1 Promotes Migration and Invasion of Osteosarcoma Cells Through the FOXF1/MMP-2/-9 Pathway.
FEZF1-AS1	NR_036484	154860	ENSG00000230316	NR_036484	GRCh38_7:122303658-122310077	gastric cancer	C16	NA	qPCR, RNAi, Western blot, RIP, ChIP, MTT assay etc.	gastric cancer tissues, cell lines (MGC-803, SGC-7901, AGS)	up-regulated	FEZF1-AS1 was overexpressed in gastric cancer. Further experiments revealed that knockdown FEZF1-AS1 significantly inhibited gastric cancer cells proliferation by inducing G1 arrest and apoptosis, whereas endogenous expression FEZF1-AS1 promoted cell growth. Additionally, RIP assay and RNA-pulldown assay evidenced that FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1, the first discovered demethylase.	28209170	2017	LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation.
FOXC2-AS1	FOXC2-AS1, ODRUL	103752587	ENSG00000260944	NR_125795	GRCh38_16:86565145-86567761	osteosarcoma	NA	M9180/3	qPCR, RNAi, Western blot, RNA-FISH etc.	osteosarcoma tissues, cell lines (MG63, SaoS2 and HOS)	up-regulated	FOXC2-AS1 and its antisense transcript FOXC2 are positively up-regulated in doxorubicin-resistant osteosarcoma cell lines and tissues, correlate with poor prognosis and promote doxorubicin resistance in osteosarcoma cells in vitro and in vivo. LncRNA FOXC2-AS1 may promote doxorubicin resistance in OS by increasing the expression of transcription factor FOXC2, further facilitating ABCB1 expression.	28323030	2017	Antisense lncRNA FOXC2-AS1 promotes doxorubicin resistance in osteosarcoma by increasing the expression of FOXC2.
FOXD2-AS1	NA	84793	ENSG00000237424	NR_026878	GRCh38_1:47432133-47434641	bladder cancer	C67	NA	Microarray,  qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP	bladder cancer tissues, bladder cancer cell lines (T24 and UM-UC-3)	up-regulated	FOXD2-AS1 promotes bladder cancer cell proliferation, migration, and invasion in vitro and in vivo. Microarray analysis demonstrated that FOXD2-AS1 negatively regulates the expression of Tribbles pseudokinase 3 (TRIB3), a negative regulator of Akt. Mechanistically, FOXD2-AS1 forms an RNA-DNA complex with the promoter of TRIB3, the transcriptional activity of which is subsequently repressed, and leads to the activation of Akt, which further increases the expression of E2F1, a vital transcription factor involved in the G/S transition. Interestingly, E2F1 could bind to the FOXD2-AS1 promoter region and subsequently enhance its transcriptional activity, indicating that FOXD2-AS1/Akt/E2F1 forms a feedback loop.	29445134	2018	Human NPC cell lines CNE2 and 5-8FThe long non-coding RNA FOXD2-AS1 promotes bladder cancer progression and recurrence through a positive feedback loop with Akt and E2F1.
FR165245	NA	NA	NA	NA	NA	lung adenocarcinoma	C34	M8140/3	microarray, qPCR etc.	cell lines (HCC827 and HCC827-8-1)	up-regulated	To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance.	27108960	2016	Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray.
FW340058	NA	NA	NA	NA	NA	neuroblastoma	NA	M9500/3	qPCR etc.	cell line (SH-SY5Y)	differential expression	We found that intronic and bidirectional promoter architectures are associated with rapid RA-dependent induction or repression of the corresponding lncRNAs, followed by their constant expression. At the same time, lncRNAs expressed downstream of protein-coding genes are characterized by rapid induction, followed by transcriptional repression. Quantitative RT-PCR analysis confirmed the discovered functional modes for several selected lncRNAs associated with proteins involved in cancer and embryonic development.	24555823	2013	Role of genomic architecture in the expression dynamics of long noncoding RNAs during differentiation of human neuroblastoma cells.
GAS5	GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007	60674	ENSG00000234741	NR_002578	GRCh38_1:173863900-173868882	non small cell lung cancer	C34	M8046/3	qPCR, RNAi, Western blot etc.	NSCLC tissues, cell lines (A549, H1650, H1299, H1975, SK-MES etc.)	down-regulated	The results revealed that GAS5 expression was down-regulated in cancerous tissues compared to adjacent noncancerous tissues and was highly related to tumor size and TNM stage. This correlation between GAS5 and clinicopathological parameters indicates that GAS5 might function as a tumor suppressor. Furthermore, GAS5 overexpression increased tumor cell growth arrest and induced apoptosis in vitro and in vivo.	24357161	2013	A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer.
GHET1	GHET1, lncRNA-GHET1	102723099	ENSG00000281189	NR_130107	GRCh38_7:148987527-148989432	bladder cancer	C67	NA	qPCR, RNAi, Western blot, in vitro knockdown etc.	bladder cancer tissues	up-regulated	In this study, we demonstrated that GHET1 was upregulated in bladder cancer tissues compared to adjacent normal tissues and its over-expression correlates with tumor size, advanced tumor and lymph node status, and poor survival. GHET1 knockdown suppressed the proliferation and invasion of bladder cancer cells in vitro. In the meantime, inhibition of GHET1 reversed the epithelial-mesenchymal-transition in bladder cancer cell line.	25400817	2014	Long noncoding RNA GHET1 promotes the development of bladder cancer.
H19	H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2	283120	ENSG00000130600	NR_002196	GRCh38_11:1995176-2001470	gallbladder cancer	C23.9	NA	qPCR, Western blot etc.	GBC tissues cell lines (NOZ, GBC-SD, SGC-996, and EH-GB1)	up-regulated	In vitro, both TGF-B1 and IL-6 treatment induced upregulation of H19, downregulated the protein level of E-cadherin while increased Vimentin, indicating an epithelial-mesenchymal transition (EMT) phenotype in GBC. The overexpression of H19 in GBC cells enhanced tumor invasion and promoted EMT by upregulated transcription factor Twist1. On the contrary, Loss of function studies indicated that H19 interference in GBC suppressed tumor cell invasion and promoted mesenchymal-epithelial transition (MET) via suppressing Twist expression. In vivo, the volume of the tumors in H19-inteference group was significantly decreased compared to those in the control group of nude mice. 	27073719	2015	Upregulation of H19 indicates a poor prognosis in gallbladder carcinoma and promotes epithelial-mesenchymal transition
H2A/K	NA	NA	NA	NA	NA	renal cancer	C64.9	NA	qPCR, Cell proliferation assay etc.	renal cancer tissues, cell line (HEK293T)	differential expression	Quantitative proteomic analysis indicated that the expression of mutant H2A/K lncRNAs resulted in the upregulation of many oncogenes, which promoted cell proliferation. Finally, the promotion of cell proliferation by mutant H2A/K lncRNAs (C290T, C228A and A45G) was confirmed using cell proliferation assays.	26953487	2016	H2A/K pseudogene mutation may promote cell proliferation.
HOXA11-AS	HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076	221883	ENSG00000240990	NR_002795	GRCh38_7:27168619-27171915	lung adenocarcinoma	C34	M8140/3	qPCR, Western blot, Luciferase reporter assay etc.	lung adenocarcinoma tissues, cell lines (A549, H1299, H1975, PC9 and SPC-A1)	up-regulated	Transcription factor ELK1 was demonstrated to upregulate HOXA10-AS in LAD cells through performing bioinformatics analysis and dual luciferase activity. Loss of function assays were performed in two different LAD cell lines. Silenced HOXA10-AS was proved to inhibit LAD progression by affecting cell proliferation, cell apoptosis and cell metastasis and EMT progress. Western blot analysis revealed that HOXA10-AS increased Wnt/B-catenin signaling in LAD cell lines. Finally, rescue assays were carried out to identify the biological function of HOXA10-AS-Wnt/B-catenin signaling in LAD progression. In conclusion, ELK1-induced upregulation of HOXA10-AS improved LAD progression through increasing Wnt/B-catenin signaling. 	29729275	2018	ELK1-induced upregulation of lncRNA HOXA10-AS promotes lung adenocarcinoma progression by increasing Wnt/B-catenin signaling.
HOXA11-AS	HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076	221883	ENSG00000240990	NR_002795	GRCh38_7:27184518-27189293	laryngeal squamous cell cancer	C32.3	NA	Microarray, qPCR, in vitro knockdown	LSCC tissues	up-regulated	Microarray and qRT-PCR showed that the level of HOXA11-AS was significantly higher in LSCC than that in the corresponding adjacent non-neoplastic tissues. ISH revealed that HOXA11-AS was strongly expressed in the nucleus and closely related to the T grade, neck nodal metastasis, and clinical stage. Patients with T3-4 grade, neck nodal metastasis, or advanced clinical stage presented a high HOXA11-AS expression. Kaplan-Meier analysis showed that high HOXA11-AS expression could predict a poor prognosis in LSCC patients. Furthermore, HOXA11-AS knockdown significantly inhibited the growth, migration, and invasion of LSCC cells.we speculated that HOXA11-AS might function through binding to proteins, such as transcription factors, in order to regulate the downstream genes.	29511452	2018	Expression of long non-coding RNA HOXA11-AS is correlated with progression of laryngeal squamous cell carcinoma.
HULC	HULC, HCCAT1, LINC00078, NCRNA00078	728655	ENSG00000251164	NR_004855	GRCh38_6:8435568-9294133	liver cancer	C22.0	NA	qPCR, Western blot, Luciferase reporter assay etc.	hepatocarcinoma cell lines (HepG2, Huh7, HepG2.2.15 ), hepatocarcinoma tissues	up-regulated	Interestingly, we also observed that HULC could up-regulate HMGA2 in HCC cells. Mechanistically, we found that the microRNA-186 inhibited HMGA2 expression by targeting the 3'-untranslated region (3'-UTR) of HMGA2 mRNA. Strikingly, HULC acted as a competing noncoding RNA to sequester miR-186 and thereby relieved miR-186-mediated HMGA2 repression. Previously, our group reported that HULC could be up-regulated by hepatitis B virus X protein (HBx) through transcription factor CREB. HULC interacted with the 5-untranslated region (5-UTR) of CLOCK mRNA via complementary base pairing, resulting in the elevation of CLOCK expression. 	28765279	2017	The long noncoding RNA HULC promotes liver cancer by increasing the expression of the HMGA2 oncogene via sequestration of the microRNA-186.
HULC	HULC, HCCAT1, LINC00078, NCRNA00078	728655	ENSG00000251164	NR_004855	GRCh38_6:8435568-9294133	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, Cell proliferation assay etc.	cell lines (HepG2, SNU-449, and SK-Hep-1)	up-regulated	Sp1, Sp3 and Sp4 transcription factors regulate HULC and other lncRNAs in HCC cells. Sp proteins and HULC regulate HCC cell proliferation, survival, migration/invasion. Knockdown of Sp1 and HULC inhibit HCC cancer cell migration and invasion	26317792	2015	Specificity protein (Sp) transcription factors and metformin regulate expression of the long non-coding RNA HULC.
LINC00152	CYTOR, C2orf59, LINC00152, NCRNA00152	112597	ENSG00000222041	NR_024204	GRCh38_2:87454781-87636740	gallbladder cancer	C23.9	NA	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay etc.	GBC tissues, cell lines (EH-GB2, GBC-SD, NOZ, SGC-996)	up-regulated	In this study, we report that the long non-coding RNA LINC00152 is significantly upregulated in GBC tissues and cell lines. The high LINC00152 levels correlated positively with tumor status progression, lymph node invasion and TNM stage advancement. Functionally, we revealed that LINC00152 dramatically promoted cell proliferation, metastasis and inhibited apoptosis in vitro. In vivo, LINC00152 overexpression significantly promoted tumor growth. Mechanistic analyses indicated that LINC00152 could participate in the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway, and transcription factor specificity protein 1 (SP1) induces its overexpression.	27829993	2016	Upregulation of long non-coding RNA LINC00152 by SP1 contributes to gallbladder cancer cell growth and tumor metastasis via PI3K/AKT pathway.
LINC00441	LINC00441, ncRNA-RB1	NA	ENSG00000231473	NA	GRCh38_13:48296513-48303661	hepatocellular carcinoma	C22.0	M8170/3	qPCR, ChIP, Luciferase reporter assay, RNA pull-down assay etc.	HCC tissues	up-regulated	We found that aberrant upregulated intranuclear Linc00441 was reversely correlated with RB1 expression in human HCC samples. The gain- and loss-of-function investigation revealed that Linc00441 could promote the proliferation of HCC cells in vitro and in vivo with an apoptosis suppression and cell cycle rearrangement. Furthermore, RNA pull-down assay indicated the decreased level of RB1 induced by Linc00441 was associated with the incidental methylation by DNMT3A recruited by Linc00441. On the contrary, the transcription factor (TCF-4) enhanced H3K27 acetylation and direct transcription factor for Linc00441 was responsible for the upregulation of Linc00441 in HCC.	28300839	2017	Bidirectional transcription of Linc00441 and RB1 via H3K27 modification-dependent way promotes hepatocellular carcinoma.
LINC00461	NA	645323	ENSG00000245526	NR_024384	GRCh38_5:88507546-88691041	glioma	NA	M9380/3	qPCR	glioma tissues	up-regulated	Taken together, our results demonstrate that LINC00461 is important for glioma progression affecting cell proliferation, migration and invasion via MAPK/ERK, PI3K/AKT, and possibly other signaling pathways.The PI3K/AKT signaling pathway plays fundamental roles in regulating cellular processes such as cell proliferation, survival, and migration [53]. Our studies found that LINC00461 positively affects both MAPK/ERK and PI3K/AKT pathways.  CyclinD1 binds to CDK4 and CDK6 (cyclin-dependent kinase 4/6) to phosphorylate retinoblastoma protein and activate the transcription factor E2F-1. In this study, we have found that LINC00461 regulates miRNA miR-9, which is the mature form of miR-9-2 gene. The sequence of miR-9-2 is included in the sequence of LINC00461.	29137410	2017	LINC00461, a long non-coding RNA, is important for the proliferation and migration of glioma cells.
LINC00668	NA	400643	ENSG00000265933	NR_034100	GRCh38_18:6919496-6929966	gastric cancer	C16	NA	qPCR, Western blot, RIP, Luciferase reporter assay etc.	gastric cancer tissues, cell lines (SGC-7901, BGC-823, MGC-803)	up-regulated	By utilizing publicly available lncRNAs expression profiling data and integrating analyses, we screened out LINC00668, whose expression is significantly increased and correlated with outcomes in gastric cancer (GC). Further experiments revealed that LINC00668 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations showed that LINC00668 was a direct transcriptional target of E2F transcription factor 1 (E2F1). We further demonstrated that LINC00668 was associated with PRC2 and that this association was required for epigenetic repression of cyclin-dependent protein kinase inhibitors (CKIs), including p15, p16, p21, p27 and p57, thus contributing to the regulation of the gastric cancer cell cycle.	27036039	2015	E2F1-induced upregulation of long noncoding RNA LINC00668 predicts a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically silencing of CKIs
LINC00673	LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1	100499467	NA	NR_036488	GRCh38_17:72403322-72592804	melanoma	NA	M8720/3	qPCR, Flow cytometry assay, RNA pull-down assay etc.	cell lines (A375, HEK293T)	up-regulated	Increased expression of this lncRNA, SLNCR1, mediates melanoma invasion through a highly conserved sequence similar to that of the lncRNA SRA1. Using a sensitive technique we term RATA (RNA-associated transcription factor array), we show that the brain-specific homeobox protein 3a (Brn3a) and the androgen receptor (AR) bind within and adjacent to SLNCR1's conserved region, respectively. SLNCR1, AR, and Brn3a are specifically required for transcriptional activation of matrix metalloproteinase 9 (MMP9) and increased melanoma invasion.	27210747	2016	The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.
LINC00963	LINC00963	100506190	ENSG00000204054	NR_038955	GRCh38_9:129483451-129513686	non small cell lung cancer	C34	M8046/3	qPCR, Northern blot, RIP etc.	cell lines (H1299, H292 )	up-regulated	Elevated expression of LINC00963 (MetaLnc9) in human NSCLC specimens correlated with poor prognosis, promoted migration and invasion of NSCLC cells in vitro, and enhanced lung metastasis formation in vivo. Mechanistic investigations showed that MetaLnc9 interacted with the glycolytic kinase PGK1 and prevented its ubiquitination in NSCLC cells, leading to activation of the oncogenic AKT/mTOR signaling pathway. MetaLnc9 also interacted with P54nrb/NonO (NONO) to help mediate the activity of CRTC, a co-activator for the transcription factor CREB, reinforcing a positive feedback loop for metastasis. Taken together, our results establish MetaLnc9 as a driver of metastasis and a candidate therapeutic target for treating advanced NSCLC.	28923857	2017	MetaLnc9 Facilitates Lung Cancer Metastasis via a PGK1-Activated AKT/mTOR Pathway
LINC01296	DUXAP9, LINC01296	NA	ENSG00000225210	NA	GRCh38_14:19062316-19131167	colorectal cancer	C19.9	NA	qPCR, Western blot etc.	CRC tissues	up-regulated	Our results showed lncRNA-CTD903 expression was strongly upregulated in 115 CRC patients, comparing to adjacent normal tissues. CTD903 was proven to be an independent predicted factor of favorable prognosis in CRC patients by using multivariate Cox proportional hazards model. After knockdown of CTD903 in RKO and SW480, both cell invasion and migration increased, and cells exhibited EMT-like appearance, along with reduced adhering ability. Moreover, overexpression of CTD903 in DLD1 and HCT116 reversed these phenotypes. Furthermore, downregulation of CTD903 enhanced Wnt/B-catenin activation and subsequently increased transcription factors (Twist and Snail) expression, along with increased mesenchymal marker Vimentin and decreased epithelial marker ZO-1 level, while overexpressed CTD903 confirmed these associations.	27035092	2016	Overexpression of long non-coding RNA-CTD903 inhibits colorectal cancer invasion and migration by repressing Wnt/B-catenin signaling and predicts favorable prognosis
LINC01503	lnc-PPP2R4-5	100506119	ENSG00000233901	NR_120685	GRCh38_9:129332300-129359538	squamous cell carcinoma	NA	M8070/3	RNA-seq, Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RNAi, RIP	non-tumor esophageal tissues, cell lines (OE33 and FLO-1, TE7, TE5 and KYSE510, KYSE30 )	up-regulated	High levels in SCCs correlated with shorter survival times of patients. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. Expression of LINC01503 in ESCC cell lines increased their proliferation, colony formation, migration, and invasion. Knockdown of LINC01503 in SCC cells reduced their proliferation, colony formation, migration, and invasion, and the growth of xenograft tumors in nude mice. Expression of LINC01503 in ESCC cell lines reduced ERK2 dephosphorylation by DUSP6, leading to activation of ERK signaling via MAPK.	29454790	2018	Increased Expression of the Long Non-Coding RNA LINC01503, Regulated by TP63, in Squamous Cell Carcinoma and Effects on Oncogenic Activities of Cancer Cell Lines.
LINC01638	NA	105372978	ENSG00000233521	NA	GRCh38_22: 27221349-27224727	breast cancer	C16	NA	qRT-PCR, Western blot assay, ChIP, Luciferase reporter assay, RIP	cell lines (MCF-10A, T47D, MCF7, BT474, SKBR3, ZR-75-30, ZR-75-1, MDA-MB-231, BT549, and HCC1937),  fresh breast tumor and adjacent non-cancerous breast tissue	up-regulated	LINC01638 is highly expressed in TNBC tissues and cells.Mechanistically, LINC01638 interacts with c-Myc to prevent SPOP-mediated c-Myc ubiquitination and degradation. C-Myc transcriptionally enhances MTDH (metadherin) expression and subsequently activates Twist1 expression to induce EMT. Analysis of the epithelial marker E-cadherin and mesenchymal markers Vimentin and EMT-associated transcription factor Twist1 revealed that LINC01638 knockdown increased E-cadherin and reduced Vimentin and Twist1 expression at the mRNA (Fig. 2g) and protein (Fig. 2h) levels in MDA-MB-231 and BT549 cells, whereas LINC01638 overexpression showed an inverse effect in T47D cells (Fig. 2g, h).	30002443	2018	LINC01638 lncRNA activates MTDH-Twist1 signaling by preventing SPOP-mediated c-Myc degradation in triple-negative breast cancer.
LINC-PINT	LINC-PINT, LincRNA-Pint, MKLN1-AS1, PINT	378805	ENSG00000231721	NR_015431	GRCh38_7:130938963-131110176	lung adenocarcinoma	C34	M8140/3	qPCR, microarry, RIP etc.	cell lines (HCT116, A549)	down-regulated	Here we characterize the function of the p53-regulated human lncRNA LINC-PINT in cancer. We find that LINC-PINT is downregulated in multiple types of cancer and acts as a tumor suppressor lncRNA by reducing the invasive phenotype of cancer cells. A cross-species analysis identifies a highly conserved sequence element in LINCPINT that is essential for its function. This sequence mediates a specific interaction with PRC2, necessary for the LINC-PINT-dependent repression of a pro-invasion signature of genes regulated by the transcription factor EGR1.	29078818	2017	The human lncRNA LINC-PINT inhibits tumor cell invasion through a highly conserved sequence element
linc-ROR	LINC-ROR, ROR, lincRNA-RoR	100885779	ENSG00000258609	NR_048536	GRCh38_18:57054558-57072119	gastric cancer	C16	NA	qPCR, RNAi, Western blot, MTT assay etc.	gastric cancer tissues, cell line (MKN-45)	up-regulated	lncRNA ROR was highly expressed in CD133+ GCSCs. Overexpression of lncRNA ROR significantly increased, but knockdown of lncRNA ROR inhibited the proliferation and invasion of GCSCs. Most importantly, lncRNA ROR led to upregulation of several key stemness transcriptional factors, such as OCT4, SOX2, and NANOG, as well as CD133 GCSC.	27602437	2016	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell.
LncZic2	NA	NA	ENSG00000043355	NA	GRCh38_13:99981772-99986773	liver cancer	C22.0	NA	qPCR, Western blot, in vitro knockdown etc.	liver cancer tissues		LncZic2 is required for the self-renewal of liver TICs in a ZIC2-independent manner. LncZic2 drove the expression of myristoylated alanine-rich protein kinase C substrate (MARCKS) and  MARCKS-like 1 (MARCKSL1), whose expression levels were increased during liver tumorigenesis and liver TIC self-renewal. Mechanistically, lncZic2 interacted with BRM/SWI2-related gene 1 (BRG1) and recruited this transcriptional regulator  to the promoters of the MARCKS and MARCKSL1 gene, which activated expression of these genes. Moreover, we noted that depletion of lncZic2 and BRG1 decreases MARCKS and MARCKSL1 expression and diminishes liver TIC levels. In conclusion, LncZic2 is required for the self-renewal of liver TICs by up-regulating MARCKS and MARCKSL1 gene expression via the transcription factor BRG1. 	29588366	2018	The long noncoding RNA lncZic2 drives the self-renewal of liver tumor-initiating  cells via the protein kinase C substrates MARCKS and MARCKSL1.  
LOC344887	NMRAL2P, NMRAL1P1	344887	ENSG00000171658	NA	GRCh38_3:185959943-185980872	gallbladder cancer	C23.9	NA	qPCR, RNAi, Western blot, CCK-8 assay etc.	GBC tissues, cell lines (NOZ, H69, SGC-996)	up-regulated	Loc344887 was upregulated significantly after ectopic expression of nuclear factor Nrf2 in GBC cells. Downregulation of Loc344887 in GBC cells suppressed cell proliferation, blocked cells in G0/S phase, and decreased the migration and invasion cell numbers. In addition, downregulation of Loc344887 decreased the expression of transcription factor Twist, mesenchymal marker Vimentin, and N-cadherin and increased the expression of epithelial maker E-cadherin, which could prompt a mesenchymal-to-epithelial transition phenotype.	28245089	2017	The NmrA-like family domain containing 1 pseudogene Loc344887 is amplified in gallbladder cancer and promotes epithelial-mesenchymal transition.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	multiple myeloma	C42.1	M9732/3	qPCR, RNAi, Luciferase reporter assay, ELISA etc.	bone marrow	up-regulated	The expression of MALAT1 was assessed by quantitative qPCR. Consistently higher expression level of MALAT1 was found in MSCs from all 25 patient samples relative to that from healthy donors. lncRNA MALAT1 directly interacted with Sp1 and LTBP3 promoter to increase expression of LTBP3 gene. The specificity and efficiency of activation were ensured by the formation of a stable complex between MALAT1 and the LTBP3 promoter, direct interaction of MALAT1 with Sp1 and recruitment of Sp1 to the promoter.	25187517	2014	Activation of LTBP3 gene by a long noncoding RNA (lncRNA) MALAT1 transcript in mesenchymal stem cells from multiple myeloma.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	Ewing sarcoma	NA	M9260/3	microarray, qPCR, Cell transfection, ChIP, Luciferase reporter assay etc.	cell lines (SKNMC, A673, TC32, TC71, SKES1, EW8, TTC-446, EWS502 and CADO-106 ES1)	up-regulated	MALAT1 is highly 267 expressed both in EWS tumor tissues and cell lines. MALAT1 was identified to be dependent on SYK-mediated signaling. Moreover, c-MYC, a SYK-promoted gene, bound to the promoter of MALAT1 and transcriptionally activated MALAT1, which further promoted the proliferation of EWS cells.	28336564	2017	Identification of a Novel SYK/c-MYC/MALAT1 Signaling Pathway and Its Potential Therapeutic Value in Ewing Sarcoma.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	monocytic leukemia	NA	M9860/3	qPCR, Western blot	leukemia cell lines (U-937 (catalog no. TCHu159), THP-1 (catalog no. TCHu 57))	up-regulated	Taken together, these findings suggest that high MALAT-1 expression is closely associated with poor prognosis in M5 patients and may play a role in leukemia cell proliferation and apoptosis, and may serve as a promising theranostic marker. We found that MALAT-1 expression in patients with acute monocytic leukemia (M5) was significantly increased when compared with that of healthy controls, and the overall survival of M5 patients with high MALAT-1 expression was markedly reduced when compared with the overall survival of patients with low MALAT-1 expression. MALAT-1 knockdown was found to induce upregulated protein expression of cyclin E and cyclin-dependent kinase 2 (CDK2) by silencing tumor suppressor gene p53 and activating transcription factor E2F, as a consequence of G1/S phase transition to G2 phase (29). 	28713913	2017	Upregulation of long non-coding RNA MALAT-1 confers poor prognosis and influences cell proliferation and apoptosis in acute monocytic leukemia.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	glioblastoma multiforme	NA	M9440/3	qRT-PCR, in vitro knockdown, RNAi	GBM cell lines (U87, T98G and LN-18, U251)	up-regulated	Importantly, our nanocomplex is able to target CSCs that are considered to be the prime culprits in therapeutic resistance and recurrence of GBM. Attenuation of MALAT1 by RNA interference significantly lowered the growth, motility and stemness of GBM cells. In addition, silencing of MALAT1 clearly improved the sensitivity of GBM cells to chemotherapeutic agents including the current first-line therapy of GBM [temozolomide (TMZ)]. In animal models of GBM, tumor involution with a modest but statistically significant survival benefit was achieved with concurrent treatment of TMZ and nanocomplex-mediated silencing of MALAT1.Expressions of both OCT4 and NANOG, transcription factors known to maintain pluripotency and self-renewal of embryonic stem cells, were significantly reduced (34.2% and 20.2%, respectively) after scL-siMAL treatment.	29202181	2018	Targeted nanocomplex carrying siRNA against MALAT1 sensitizes glioblastoma to temozolomide.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	oral squamous cell carcinoma	C06.9	M8070/3 	qPCR, RNAi, Western blot etc.	OSCC tissues, cell lines (Tscca, Tca8113P160, Tca8113, Hep-2)	up-regulated	We found that MALAT1 is overexpressed in OSCC tissues compared to normal oral mucosa by real-time PCR. MALAT1 served as a new prognostic factor in OSCC patients. When knockdown by small interfering RNA (siRNA) in OSCC cell lines TSCCA and Tca8113, MALAT1 was shown to be required for maintaining epithelial-mesenchymal transition (EMT) mediated cell migration and invasion. Western blot and immunofluorescence staining showed that MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both nucleus and cytoplasm levels of B-catenin and NF-B were attenuated, while elevated MALAT1 level triggered the expression of B-catenin and NF-B. More importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth in vivo.	26522444	2015	Long Non Coding RNA MALAT1 Promotes Tumor Growth and Metastasis by inducing Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	liver cancer	C22.0	NA	microarray, qPCR, Western blot, RIP, Luciferase reporter assay etc.	liver cancer tissues, cell lines (HepG2, Bel-7402, SMMC-7721, HEK-293T etc.)	differential expression	Yes-associated protein (YAP), which up-regulated Malat1 expression at both transcriptional and post-transcriptional levels, whereas serine/arginine-rich splicing factor 1 (SRSF1) played an opposing role. SRSF1 inhibited YAP activity by preventing its co-occupation with TCF/B-catenin on the Malat1 promoter. In contrast, overexpression of YAP impaired the nuclear retention of both SRSF1 and itself via an interaction with Angiomotin (AMOT). This effect removed the inhibitory role of SRSF1 on Malat1 in the nucleus.	24468535	2014	Mutual inhibition between YAP and SRSF1 maintains long non-coding RNA, Malat1-induced tumourigenesis in liver cancer.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	prostate cancer	C61.9	NA	microarray, qPCR etc.	cell lines (UMR-106 and PC3)	up-regulated	The qPCR data showed a ~6-fold increase in MALAT1 expression in PC3 cells co-cultured with UMR osteoblasts compared to PC3 monocultures. Treatment with recombinant SOST resulted in ~5.6-fold reduction in MALAT1 expression, suggesting that Sost in the tumor microenvironment may have an inhibitory effect on MALAT1 and down-regulation of Sost in the bone microenvironment may enhance MALAT1 expression in prostate cancer.	27600237	2016	Cancer-Osteoblast Interaction Reduces Sost Expression in Osteoblasts and Up-Regulates lncRNA MALAT1 in Prostate Cancer.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	multiple myeloma	C42.1	M9732/3	qPCR etc.	myeloma tissues	up-regulated	The upregulation of MALAT1 appeared associated in MM patients with molecular pathways involving cell cycle regulation, p53-mediated DNA damage response, and mRNA maturation processes.	26895470	2016	Distinct lncRNA transcriptional fingerprints characterize progressive stages of multiple myeloma.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	colorectal cancer	C19.9	NA	qPCR etc.	CRC tissues	up-regulated	The MALAT1 levels in cancerous tissues were 2.26 times higher than those measured in noncancerous tissues, and this difference was statistically significant. Based on their expression level of MALAT1, the patients were divided into a high MALAT1 expression group and a low expression group. Patients with tumours harbouring higher expression of MALAT1 showed a significantly worse prognosis with a HR of 2.863 for DFS and 3.968 for OS. Furthermore, patients with perineural invasion demonstrated significantly worse DFS and OS than those without perineural invasion.	25031737	2014	High expression of lncRNA MALAT1 suggests a biomarker of poor prognosis in colorectal cancer.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	pancreatic cancer	C25	NA	qPCR, RNAi, Western blot, RIP, Flow cytometry assay, Cell proliferation assay etc.	pancreatic cancer tissues, cell lines (CFPAC-1, SW1990, AsPC-1)	up-regulated	And knockdown of MALAT-1 upregulated E-cadherin mRNA expression in pancreatic cancer cell lines. Therefore, we hypothesized that EZH2 might be recruited by MALAT-1 to synergistically repress E-cadherin. To test this hypothesis, we first asked whether MALAT-1 bound to EZH2 using a RNA Immunoprecipitation (RIP) assay. There was an average of 14- and 18- fold enrichment for MALAT-1 in the AsPC-1 and CFPAC-1 cells over-expressing EZH2, respectively, as compared to the IgG group. These results suggest that MALAT-1 is physically associated with the EZH2, and silencing EZH2 could increase E-cadherin transcription.	26848980	2016	EZH2 promotes cell migration and invasion but not alters cell proliferation by suppressing E-cadherin, partly through association with MALAT-1 in pancreatic cancer.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	osteosarcoma	NA	M9180/3	qPCR etc.	osteosarcoma tissues	up-regulated	The expression of MALAT-1, IMPDH2, FTL and RHOA significantly correlated with response to chemotherapy. Expression of all four genes was increased in the poor responder group that are valuable markers for the prediction of osteosarcoma therapy outcome. Especially IMPDH2 and FTL are promising candidates for the stratification of osteosarcoma patients into low- and high-risk groups. Owing to their involvement in drug action these genes may further be potential targets for the modulation of drug sensitivity.	17660802	2007	Prognostic significance of drug-regulated genes in high-grade osteosarcoma.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	colorectal cancer	C19.9	NA	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc.	CRC tissues, cell line (LoVo)	up-regulated	Using in situ hybridization, we found there was higher expression of MALAT1 in the CRC than the adjacent normal colorectal tissue. We next conducted correlation analysis between MALAT1 expression and clinicopathological characteristics of CRC. A statistically significant association was observed between MALAT1 expression and extent of metastasis and invasion. In contrast to adjacent normal tissues, the MALAT1 expression in CRC tissues resected from patients with metastatic diseases was higher than those with no metastasis. 	24244343	2013	Resveratrol inhibits invasion and metastasis of colorectal cancer cells via MALAT1 mediated Wnt/B-Catenin signal pathway.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	breast cancer	C50	NA	qPCR, in vitro knockdown etc.	cell lines (MDA-MB-231 and MCF7)	up-regulated	We demonstrate that MALAT1 facilitates cell proliferation, tumor progression and metastasis of triple-negative breast cancer (TNBC) cells despite having a comparatively lower expression level than ER or HER2-positive breast cancer cells. Assessment of the prognostic significance of MALAT1 in human breast cancer (n=1992) revealed elevated MALAT1 expression was associated with decreased disease-specific survival in ER negative, lymph node negative patients of the HER2 and TNBC molecular subtypes. Multivariable analysis confirmed MALAT1 to have independent prognostic significance in the TNBC lymph node negative patient subset.	27250026	2016	Functional and prognostic significance of long non-coding RNA MALAT1 as a metastasis driver in ER negative lymph node negative breast cancer.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	gastric cancer	C16	NA	qPCR, RNAi, Western blot etc.	gastric cancer tissues, cell lines (SGC-7901, BGC823, AGS and MKN45)	up-regulated	MALAT-1 was upregulated in GC cell lines and tissues. Moreover, MALAT-1 expression was higher in the high-metastatic-potential GC cell line SGC7901M than in the low-metastatic-potential GC cell line SGC7901NM. Silencing of MALAT-1 inhibited GC cell migration and invasion. In addition, suppressing MALAT-1 expression resulted in a decrease in the expression of the Epithelial-mesenchymal transition-associated marker vimentin and an increase in the expression of E-cadherin at both the mRNA and protein levels.	28276823	2017	The role of MALAT-1 in the invasion and metastasis of gastric cancer.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	cervical cancer	C53	NA	qPCR, RNAi, Western blot etc.	cervical cancer tissues, cell lines (CaSki, HeLa, and SiHa)	up-regulated	In this study, we found that MALAT1 expression levels were significantly increased in cervical cancer (CC) cells and tissues. The down-regulation of MALAT1 by shRNA in CC cells inhibited the invasion and metastasis in vitro and in vivo. Microarray analysis showed that the knockdown of MALAT1 up-regulated the epithelial markers E-cadherin and ZO-1, and down-regulated the mesenchymal markers B-catenin and Vimentin.	26798987	2016	Down-regulation of MALAT1 inhibits cervical cancer cell invasion and metastasis by inhibition of epithelial-mesenchymal transition.
MALAT1	MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853	378938	ENSG00000251562	NR_002819	GRCh38_11:65497688-65506516	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, ChIP, Cell proliferation assay etc.	HCC tissues, cell lines (HepG2, SMMC-7721, Bel-7402, MHCC97H, and HCC-LM3)	up-regulated	In addition, hypoxia-inducible factor (HIF)-2a is up-regulated in HCCs, and MALAT1 and HIF-2a have a positive correlation in HCC tissues. During the malignant transformation of human hepatic epithelial (L-02) cells induced by a low concentration (2.0 μM) of arsenite, MALAT1 and HIF-2a are increased. In addition, arsenite-induced MALAT1 causes disassociation of the von Hippel-Lindau (VHL) protein from HIF-2a, therefore, alleviating VHL-mediated HIF-2a ubiquitination, which causes HIF-2a accumulation. In turn, HIF-2a transcriptionally regulates MALAT1, thus forming a positive feedback loop to ensure expression of arsenite-induced MALAT1 and HIF-2a, which are involved in malignant transformation. Moreover, MALAT1 and HIF-2a promote the invasive and metastatic capacities of arsenite-induced transformed L-02 cells and in HCC-LM3 cells.	26735578	2016	A MALAT1/HIF-2a feedback loop contributes to arsenite carcinogenesis.
MA-linc1	LINC01024, MA-linc1	100505636	ENSG00000245146	NR_102739	GRCh38_5:140072857-140108630	lung cancer	C34	NA	qPCR, RNAi, Western blot etc.	cell line (H1299)	up-regulated	We employed qPCR to analyze MA-linc1 levels in four cell lines: U2OS and H1299 cells, as well as the human embryonic lung fibroblasts, WI38, and another human osteosarcoma cell line, SAOS-2, each expressing the conditionally active E2F1. This analysis demonstrated that activation of the ectopic E2F1 resulted in a significant increase in MA-linc1 RNA levels in all four cell lines.	26337085	2015	A novel mitosis-associated lncRNA, MA-linc1, is required for cell cycle progression and sensitizes cancer cells to Paclitaxel.
MA-linc1	LINC01024, MA-linc1	100505636	ENSG00000245146	NR_102739	GRCh38_5:140072857-140108630	osteosarcoma	NA	M9180/3	qPCR, RNAi, Western blot etc.	cell lines (U2OS, SAOS-2)	up-regulated	We employed qPCR to analyze MA-linc1 levels in four cell lines: U2OS and H1299 cells, as well as the human embryonic lung fibroblasts, WI38, and another human osteosarcoma cell line, SAOS-2, each expressing the conditionally active E2F1. This analysis demonstrated that activation of the ectopic E2F1 resulted in a significant increase in MA-linc1 RNA levels in all four cell lines.	26337085	2015	A novel mitosis-associated lncRNA, MA-linc1, is required for cell cycle progression and sensitizes cancer cells to Paclitaxel.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	multiple myeloma	C42.1	M9732/3	qPCR, RNAi, Lentiviral infection, Western blot etc.	bone marrow	up-regulated	We observed that MEG3 knockdown significantly reduced the expression of key osteogenic markers, including Runt-related transcription factor 2, osterix, and osteocalcin, while overexpression of MEG3 enhanced their expression. Additionally, MEG3 knockdown decreased BMP4 transcription. Here we showed that MEG3 was critical for SOX2 transcriptional repression of the BMP4. MEG3, which is located near the BMP4 gene, could dissociate the transcription factor SOX2 from the BMP4 promoter. A stable complex containing the MEG3, SOX2, and the SOX2 consensus site of BMP4 suggested that MEG3 activated transcriptional activity by directly influencing SOX2 activity.	25753650	2015	Upregulation of lncRNA MEG3 Promotes Osteogenic Differentiation of Mesenchymal Stem Cells From Multiple Myeloma Patients By Targeting BMP4 Transcription.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	colon cancer	C18	NA	qPCR, Western blot, Northern blot, ChIP etc.	cell lines (HCT116, U2OS)	down-regulated	We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter. Interestingly, MEG3 does not stimulate p21(CIP1) expression, suggesting that MEG3 can regulate the specificity of p53 transcriptional activation. p53 degradation is mainly mediated by the mouse double minute 2 homolog (MDM2). We found that MDM2 levels were down-regulated in cells transfected with MEG3, suggesting that MDM2 suppression contributes at least in part to p53 accumulation induced by MEG3. Finally, we found that MEG3 is able to inhibit cell proliferation in the absence of p53.	17569660	2007	Activation of p53 by MEG3 non-coding RNA.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	osteosarcoma	NA	M9180/3	qPCR, Western blot, Northern blot, ChIP etc.	cell lines (HCT116, U3OS)	down-regulated	We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter. Interestingly, MEG3 does not stimulate p21(CIP1) expression, suggesting that MEG3 can regulate the specificity of p53 transcriptional activation. p53 degradation is mainly mediated by the mouse double minute 2 homolog (MDM2). We found that MDM2 levels were down-regulated in cells transfected with MEG3, suggesting that MDM2 suppression contributes at least in part to p53 accumulation induced by MEG3.	17569660	2007	Activation of p53 by MEG3 non-coding RNA.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	lung cancer	C34	NA	microarray, qPCR, Cell transfection, Western blot etc.	cell lines (A549 and SK-MES-1)	down-regulated	MEG3 levels also were suppressed in A549 lung cancer cells compared with normal human bronchial epithelial (NHBE) cells, and, similar to the TKO cells, re-constitution of MEG3 led to a decrease in cell proliferation and elevated apoptosis. Activation of pRb by treatment of A549 and SK-MES-1 cells with palbociclib, a CDK4/6 inhibitor, increased the expression of MEG3 in a dose-dependent manner, while knockdown of pRb/p107 attenuated this effetc.	27832204	2016	Expression of the lncRNA Maternally Expressed Gene 3 (MEG3) Contributes to the Control of Lung Cancer Cell Proliferation by the Rb Pathway.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	lung cancer	C34	NA	qPCR, RNAi, Western blot, MTT assay etc.	cell lines (A549 and A549/DDP)	down-regulated	The present study detected that the expression levels of Meg3 were significantly lower in cisplatin-resistant A549/DDP lung cancer cells, compared with those in parental A549 cells. Furthermore, upregulation of Meg3 was able to re-sensitize the A549/DDP cells to cisplatin in vitro. Whereas downregulation of Meg3, by RNA interference, decreased the sensitivity of A549 cells to cisplatin. The results of the present study also demonstrated that the Meg3-mediated chemosensitivity enhancement was associated with the induction of cell-cycle arrest and increased apoptosis, through regulation of p53, B-catenin and survivin, which is a target gene of the WNT/B-catenin signaling pathway.	26059239	2015	Downregulation of Meg3 enhances cisplatin resistance of lung cancer cells through activation of the WNT/B-catenin signaling pathway.
MEG3	MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1	55384	ENSG00000214548	NR_002766	GRCh38_14:100779410-100861031	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Western blot, Flow cytometry assay, MTT assay etc.	cell line (HepG2)	differential expression	Ectopic expression of MEG3 inhibited HepG2 cell proliferation in vitro and in vivo, and also induced apoptosis. Ectopic expression of MEG3 increased ER stress-related proteins 78-kDa glucose-regulated protein (GRP78), inositol-requiring enzyme 1 (IRE1), RNA-dependent protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase-3, as well as p53 and NF-kB expression accompanied by NF-kB translocation from the cytoplasm to the nucleus. Furthermore, inhibition of NF-kB with Bay11-7082 decreased p53 expression in the MEG3-transfected cells.	27432655	2016	Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis.
MIAT	MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT	440823	ENSG00000225783	NR_003491	GRCh38_22:26646428-26676475	chronic lymphocytic leukemia	NA	M9823/3	qPCR, RNAi, Western blot, Cell proliferation assay etc.	CLL tissues, leukemia/lymphoma cell lines	up-regulated	MIAT expression was upregulated in breast cancer cell lines and tissues.MIAT acted as a competing endogenous RNA (ceRNA) to regulate the expression of dual specificity phosphatase 7 (DUSP7) by taking up miR-155-5p in breast cancer. There were positive correlation between MIAT and DUSP7 expression in breast cancer patients.MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p in breast cancer. MIAT was specifically up-regulated in the plasma and aqueous humor of cataract patients.	27527866	2016	Upregulation of long noncoding RNA MIAT in aggressive form of chronic lymphocytic leukemias.
MINCR	MINCR, LINC01604	100507316	ENSG00000253716	NR_120682	GRCh38_8:143280161-143281690	B-cell lymphoma	NA	M9591/3	qPCR, RNAi, Lentiviral infection, ChIP etc.	cell lines (hT-RPE-MycER)	up-regulated	We focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Differential gene expression analysis after RNAi showed a significant enrichment of cell cycle genes among the genes down-regulated after MINCR knockdown. Interestingly, these genes are enriched in MYC binding sites in their promoters, suggesting that MINCR acts as a modulator of the MYC transcriptional program. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes.	26351698	2015	MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells.
MIR22HG	MIR22HG, C17orf91	84981	ENSG00000186594	NR_028502	GRCh38_17:1711493-1717174	lung squamous cell carcinoma	C34	M8070/3	microarray, qPCR etc.	LSCC tissues	down-regulated	Finally, to ensure that our results was not population and technical specific, we assessed the expression level of 6 lncRNAs using qRT-PCR in all 47 paired lung SQCC tumors and NTL tissues. These lncRNAs were randomly chosen from differentially expressed lncRNA transcripts. In consistent with microarray analysis, the results demonstrated that all the 6 lncRNAs were down-regulated in lung SQCC tissues vs. matched non-tumor tissues.	26159226	2015	Genome-scale long noncoding RNA expression pattern in squamous cell lung cancer.
MNX1-AS1	MNX1-AS1, CCAT5	645249	ENSG00000243479	NR_038835	GRCh38_7:157010805-157016426	colorectal cancer	C19.9	NA	microarray, qPCR, Luciferase reporter assay etc.	CRC tissues, cell lines (HCT116, RKO, HT29, SW620 etc.)	up-regulated	Of the seletced lncRNAs, four lncRNAs named CCAT3, CCAT4, CCAT5, and CCAT6 (also named MYCLo-2) are upregulated in CRC cell lines, and two lncRNAs named CCAT7 and CCAT8 are downregulated in CRC cell lines. MYC-regulated lncRNAs, named MYCLos. The MYC-regulated MYCLos may function in cell proliferation and cell cycle by regulating MYC target genes such as CDKN1A (p21) and CDKN2B (p15), suggesting new regulatory mechanisms of MYC-repressed target genes through lncRNAs.	25663692	2015	Role of MYC-regulated long noncoding RNAs in cell cycle regulation and tumorigenesis.
MT1DP	MT1JP, MT1, MT1J, MT1NP, MTB	NA	ENSG00000205361	NA	GRCh38_16:56643705-56644786	liver cancer	C22.0	NA	qPCR, Western blot, Luciferase reporter assay etc.	cell lines (SMMC-7721, Bel-7402, Huh7, HepG2, DLD-1, LS174T)	down-regulated	Overexpression of MT1DP resulted in reduced cell proliferation and colony formation in soft agar, but increased apoptosis in liver cancer cells, whereas knockdown of this lncRNA had the opposite effetc, indicating that MT1DP acts as a tumor suppressor. Furthermore, MT1DP was revealed as a negative regulator of Alfa-fetoprotein (AFP), a classic liver cancer tumor marker, through inhibiting protein synthesis of Forkhead box A1 (FoxA1), an important transcription factor in liver development and cancer progression.	25261601	2014	Tumor suppressor long non-coding RNA, MT1DP is negatively regulated by YAP and Runx2 to inhibit FoxA1 in liver cancer cells.
MT1JP	MT1JP, MT1, MT1J, MT1NP, MTB	NA	ENSG00000255986	NA	GRCh38_16:56635739-56637086	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, Northern blot etc.	cell lines (L02, SMMC-7721 and HepG2)	down-regulated	The results of qRT-PCR analyses showed that MT1JP is expressed at higher levels in non-cancerous than in cancerous cell lines, consistent with the results from the tissue samples. By associating with the RNA-binding protein TIAR, MT1JP enhanced the translation of the master transcription factor p53, thereby regulating a series of pathways involving p53, such as the cell cycle, apoptosis and proliferation. When MT1JP was down-regulated, the protein level of p53 declined, which in turn accelerated cell deterioration and tumor formation. Moreover, differential expression of MT1JP in cancerous and normal tissues suggests that it may be a promising prognostic marker and a therapeutic target.	26909858	2016	LncRNA MT1JP functions as a tumor suppressor by interacting with TIAR to modulate the p53 pathway.
MYCLo-4	AK098037	NA	NA	NA	NA	colorectal cancer	C19.9	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-4	AK098037	NA	NA	NA	NA	lung cancer	C34	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-4	AK098037	NA	NA	NA	NA	prostate cancer	C61.9	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	breast cancer	C50	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	colorectal cancer	C19.9	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	lung cancer	C34	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	prostate cancer	C61.9	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	breast cancer	C50	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	colorectal cancer	C19.9	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	hepatocellular carcinoma	C22.0	M8170/3	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	lung cancer	C34	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
MYCLo-5	LPP-AS2, MYCLo-5, MYCLo-6	339929	ENSG00000270959	NR_036497	GRCh38_3:188151206-188154057	prostate cancer	C61.9	NA	qPCR, Flow cytometry assay, Cell proliferation assay etc.	cell lines (HCT116, RKO, HT29, A549, PC3, MCF7 and SKBR3, SK-HEP-1 and HepG2)	down-regulated	Of the tested cell lines, MYCLo-4 was upregulated by MYC knockdown in HCT116 (CRC), RKO (CRC), HT29 (colorectal adenocarcinoma), A549 (Lung carcinoma) and PC3 (prostate cancer). The other 2 lncRNAs, MYCLo-5 and -6 were also induced by MYC repression in various cancer types such as CRC (HCT116, RKO and HT29), lung cancer (A549), prostate cancer (PC3), breast cancer (MCF7 and SKBR3) and hepatocellular carcinoma (SK-HEP-1 and HepG2). 	26003165	2015	MYC-repressed long noncoding RNAs antagonize MYC-induced cell proliferation and cell cycle progression.
NBAT1	NBAT1, CASC14, NBAT-1	729177	ENSG00000260455	NR_034143	GRCh38_6:22134957-22147193	neuroblastoma	NA	M9500/3	qPCR etc.	primary neuroblastoma tissues	down-regulated	We identified a lncRNA neuroblastoma associated transcript-1 (NBAT-1) as a biomarker significantly predicting clinical outcome of neuroblastoma. CpG methylation and a high-risk neuroblastoma associated SNP on chromosome 6p22 functionally contribute to NBAT-1 differential expression. Loss of NBAT-1 increases cellular proliferation and invasion. It controls these processes via epigenetic silencing of target genes. NBAT-1 loss affects neuronal differentiation through activation of the neuronal-specific transcription factor NRSF/REST.	25517750	2014	The risk-associated long noncoding RNA NBAT-1 controls neuroblastoma progression by regulating cell proliferation and neuronal differentiation.
nc886	VTRNA2-1, CBL-3, CBL3, MIR886, MIRN886, VTRNA2, hsa-mir-886, hvg-5, nc886, svtRNA2-1a	100126299	ENSG00000270123	NR_030583	GRCh38_5:136080470-136080597	lung adenocarcinoma	C34	M8140/3	microarray, qPCR etc.	cell lines (HCC827 and HCC827-8-1)	down-regulated	To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance.	27108960	2016	Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray.
NEAT1	NEAT1, LINC00084, NCRNA00084, TncRNA, VINC	283131	ENSG00000245532	NR_028272	GRCh38_11:65422774-65445540	leukemia	NA	M9800/3	qPCR, RNAi, Western blot, Flow cytometry assay etc.	blood, cell lines (K562, THP-1, HL-60, Jurkat)	down-regulated	NEAT1 messenger RNA (mRNA) expression levels were significantly downregulated in leukemia patient samples compared with those from healthy donors. Furthermore, NEAT1 mRNA expression was repressed in a number of leukemia cell lines, including K562, THP-1, HL-60 and Jurkat cells, compared with peripheral white blood control cells, consistent with the expression observed in patients with leukemia. In addition, the transfection of a NEAT1 overexpression plasmid into K562 and THP-1 leukemia cell lines alleviated MDR induced by cytotoxic agents, such as Alisertib and Bortezomib, through inhibition of ATP-binding cassette G2.	27446393	2016	Overexpression of lncRNA NEAT1 mitigates multidrug resistance by inhibiting ABCG2 in leukemia.
NEAT1	NEAT1, LINC00084, NCRNA00084, TncRNA, VINC	283131	ENSG00000245532	NR_028272	GRCh38_11:65422774-65445540	acute promyelocytic leukemia	NA	M9866/3	qPCR, Western blot etc.	cell lines (NB4 and 293T)	down-regulated	In this study, we performed chromatin immunoprecipitation and luciferase reporter assays  to demonstrate that C/EBP family transcription factor C/EBPB bind to and transactivate the promoter of lncRNA NEAT1 through the C/EBPB binding sites both  around -54 bp and -1453 bp upstream of the transcription start site. Moreover, the expression of C/EBPB was increased after ATRA treatment, and the binding of C/EBPB in the NEAT1 promoter was also dramatically increased. Finally, knockdown  of C/EBPB significantly reduced the ATRA-induced upregulation of NEAT1. In conclusion, C/EBPB directly activates the expression of NEAT1 through binding to  the promoter of NEAT1. Knockdown of C/EBPB impairs ATRA-induced transcriptional activation of NEAT1.	29111326	2018	C/EBPB contributes to transcriptional activation of long non-coding RNA NEAT1 during APL cell differentiation.
NEAT1	NEAT1, LINC00084, NCRNA00084, TncRNA, VINC	283131	ENSG00000245532	NR_028272	GRCh38_11:65422774-65445540	acute promyelocytic leukemia	NA	M9866/3	qPCR, Western blot etc.	blood, cell lines (NB4, NB4-R2, U937-PR9)	down-regulated	We found that NEAT1 is significantly repressed in de novo APL samples compared with those of healthy donors. We further provide evidence that NEAT1 expression was repressed by PML-RAR. Furthermore, significant NEAT1 upregulation was observed during all-trans retinoic acid (ATRA)-induced NB4 cell differentiation.	25245097	2014	Inhibition of long non-coding RNA NEAT1 impairs myeloid differentiation in acute promyelocytic leukemia cells.
NEAT1	NEAT1, LINC00084, NCRNA00084, TncRNA, VINC	283131	ENSG00000245532	NR_028272	GRCh38_11:65422774-65445540	breast cancer	C50	NA	qPCR, ISH etc.	cell lines (MCF-7, MDA-MB-231, MDAMB-468)	up-regulated	Induction of NEAT1 in hypoxia also leads to accelerated cellular proliferation, improved clonogenic survival and reduced apoptosis, all of which are hallmarks of increased tumorigenesis. Furthermore, in patients with breast cancer, high tumor NEAT1 expression correlates with poor survival, all of which are hallmarks of increased tumorigenesis.	25417700	2014	Tumor hypoxia induces nuclear paraspeckle formation through HIF-2a dependent transcriptional activation of NEAT1 leading to cancer cell survival.
NKILA	AK056098	105416157	ENSG00000278709	NR_131157	GRCh38_20:57710183-57712780	malignant melanoma	NA	M8720/3	qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc.	melanoma tissues, cell lines (M21, B16, MEL-RM, MM200, A375 and A2058)	down-regulated	NKILA was expressed at low levels in human melanoma tissues. Our results also indicated that NKILA inhibited the progression of cell proliferation, migration, and invasion, and promoted apoptosis of melanoma cells. Furthermore, qRT-PCR showed that NF-kB, which was negatively correlated with NKILA, was highly expressed in human melanoma tissues. Moreover, our results indicated that NKILA inhibited the carcinogenesis of melanoma cells through the inhibition of NF-B in vitro. More importantly, we found that NKILA suppressed the growth of melanoma tumors via NF-B in vivo.	28123845	2017	The long non-coding RNA NKILA inhibits the invasion-metastasis cascade of malignant melanoma via the regulation of NF-B.
NKILA	AK056098	105416157	ENSG00000278709	NR_131157	GRCh38_20:57710183-57712780	tongue squamous cell carcinoma	C02	M8070/3	qPCR, Western blot, ISH etc.	TSCC tissues, cell lines (CAL27, Tca8113)	down-regulated	NKILA is down-regulated in TSCC cancer tissues than that in matched adjacent noncancerous tissues. And low NKILA expression in TSCC is significantly correlated with tumor metastasis and poor patient prognosis. In vitro, overexpression of NKILA decreases TSCC cells migration and invasion. Mechanistic study shows that NKILA inhibits the phosphorylation of IkBa and NF-kB activation as well as the induction of the epithelial-mesenchymal transition (EMT) process.	27613832	2016	Long non-coding RNA NKILA inhibits migration and invasion of tongue squamous cell carcinoma cells via suppressing epithelial-mesenchymal transition.
NKILA	AK056098	105416157	ENSG00000278709	NR_131157	GRCh38_20:57710183-57712780	breast cancer	C50	NA	qPCR, RNAi, RIP etc.	breast cancer tissues	down-regulated	Importantly, NKILA is essential to prevent over-activation of NF-B pathway in inflammation-stimulated breast epithelial cells. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-B modulators to suppress cancer metastasis.	25759022	2015	A Cytoplasmic NF-B Interacting Long Noncoding RNA Blocks IB Phosphorylation and Suppresses Breast Cancer Metastasis.
NONHSAG010125	NA	NA	NA	NA	NA	clear cell renal cell carcinoma	C64.9	M8005/0	microarray, qPCR etc.	primary RCCC tissues	up-regulated	For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data.	26765468	2016	Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma.
NONHSAG019720	NA	NA	NA	NA	NA	clear cell renal cell carcinoma	C64.9	M8005/0	microarray, qPCR etc.	primary RCCC tissues	up-regulated	For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data.	26765468	2016	Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma.
NONHSAT024642	NA	NA	NA	NA	NA	clear cell renal cell carcinoma	C64.9	M8005/0	microarray, qPCR etc.	primary RCCC tissues	up-regulated	For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data.	26765468	2016	Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma.
NONHSAT066293	NA	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	up-regulated	Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results.	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
NONHSAT104436	NA	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	up-regulated	Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results.	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
NONHSAT112918	NA	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	up-regulated	To better understand the roles of lncRNAs in ESCC, we first checked the expression levels of the 4 lncRNAs (ENST00000480669, NONHSAT104436, NONHSAT126998 and NONHSAT112918). The expression of lncRNAs were quantified via RT-PCR in ESCC tissues and matched noncancerous tissues. 	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
NONHSAT123350	NA	NA	NA	NA	NA	clear cell renal cell carcinoma	C64.9	M8005/0	microarray, qPCR etc.	primary RCCC tissues	down-regulated	For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data.	26765468	2016	Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma.
NONHSAT126998	NA	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	up-regulated	To better understand the roles of lncRNAs in ESCC, we first checked the expression levels of the 4 lncRNAs (ENST00000480669, NONHSAT104436, NONHSAT126998 and NONHSAT112918). The expression of lncRNAs were quantified via RT-PCR in ESCC tissues and matched noncancerous tissues. 	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
NONHSAT142035	NA	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	down-regulated	Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results.	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
NONHSAT147911	NA	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	up-regulated	Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results.	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
NR_036468.1	CIDEA, CIDE-A	NA	NA	NA	NA	esophageal squamous cell cancer	NA	NA	microarray, qPCR etc.	ESCC tissues	down-regulated	Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results.	27035335	2016	Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma.
NR_046028	ACOT2, CTE-IA, CTE1A, MTE1, PTE2, PTE2A, ZAP128	NA	NA	NA	NA	clear cell renal cell carcinoma	C64.9	M8005/0	microarray, qPCR etc.	primary RCCC tissues	down-regulated	For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data.	26765468	2016	Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma.
OIP5-AS1	OIP5-AS1, cyrano, linc-OIP5	729082	ENSG00000247556	NR_026757	GRCh38_15:41283990-41309737	oral cancer	C06.9	NA	RNA-seq, Microarray, qPCR, Luciferase reporter assay, RIP etc.	oral tumor tissues, cell lines (FANTOM 5 and GTEx)	up-regulated	Expression analysis showed downregulation of miRNAs and upregulation of downstream target genes, particularly in undifferentiated tumors with high-level of OIP5-AS1 suggesting OIP5-AS1 could post-transcriptionally modulate the downstream target genes. Further, systematic epigenomic analysis of OIP5-AS1 promoter revealed binding motifs for MYC, NANOG and KLF4 suggesting that OIP5-AS1 could be transactivated by stemness-associated transcription factors in cancer. OIP5-AS1 overexpression in undifferentiated oral tumors may be suggestive of enhanced cancer stemness, and consequently, poor clinical outcome.	29728583	2018	LncRNA OIP5-AS1 is overexpressed in undifferentiated oral tumors and integrated analysis identifies as a downstream effector of stemness-associated transcription factors.
PACER	PACERR, PACER, PTGS2-AS1	103752588	ENSG00000273129	NR_125801	GRCh38_1:186680622-186681446	osteosarcoma	NA	M9180/3	qPCR, RNAi, Western blot, Cell proliferation assay etc.	osteosarcoma tissues, cell lines (143B, MG63, Saos-2, U2OS, hFOB1.19)	up-regulated	The results showed that PACER was overexpressed in osteosarcoma tissues and cell lines compared with normal tissues and osteoblasts, respectively. PACER knockdown inhibited the proliferation and invasion of human osteosarcoma cells. Downregulation of PACER significantly suppressed the expression of COX-2, and the effects of PACER on cell proliferation and invasion were rescued by COX-2 overexpression. 	26476537	2016	P50-associated COX-2 extragenic RNA (PACER) overexpression promotes proliferation and metastasis of osteosarcoma cells by activating COX-2 gene.
PANDAR	PANDAR, PANDA	101154753	ENSG00000281450	NR_109836	GRCh38_6:36673621-36675126	osteosarcoma	NA	M9180/3	qPCR, RNAi, Cell cycle assay etc.	cell lines (U2OS, A549, H1299, HeLa and MCF7)	up-regulated	PANDA was highly expressed in U2OS cells, and its expression was induced by DNA damage. Silencing PANDA caused arrest at the G1 phase of the cell cycle, leading to inhibition of cell proliferation. Quantitative RT-PCR showed that silencing PANDA increased mRNA levels of the cyclin-dependent kinase inhibitor p18, which caused G1 phase arrest.	28011477	2017	Long Noncoding RNA PANDA Positively Regulates Proliferation of Osteosarcoma Cells.
PANDAR	PANDAR, PANDA	101154753	ENSG00000281450	NR_109836	GRCh38_6:36673621-36675126	non small cell lung cancer	C34	M8046/3	qPCR, Western blot, RIP etc.	lung cancer tissues, cell lines (A549, SPC-A1, NCI-H1299, SK-MES-1 etc.)	down-regulated	In a cohort of 140 NSCLC patients, decreased PANDAR expression was negatively correlated with greater tumor size and advanced TNM stage. Moreover, PANDAR could serve as an independent predictor for overall survival in NSCLC. PANDAR-mediated growth regulation is in part due to the transcriptional modulation of Bcl-2 by interacting with NF-YA, thus affecting NSCLC cell apoptosis.	25719249	2015	Low expression of long noncoding RNA PANDAR predicts a poor prognosis of non-small cell lung cancer and affects cell apoptosis by regulating Bcl-2.
PANDAR	PANDAR, PANDA	101154753	ENSG00000281450	NR_109836	GRCh38_6:36673621-36675126	retinoblastoma	C69.2	M9510/3	qPCR,ChIP etc.	retinoblastoma tissues, cell lines (ARPE-19 and RB )	up-regulated	The results indicated that PANDAR was increased in RB tissues and cells, and this upregulation was associated with advanced IIRC stage, positive optic nerve invasion, and lower differentiation grade RB patients.	29778422	2018	SP1-induced upregulation of lncRNA PANDAR predicts adverse phenotypes in retinoblastoma and regulates cell growth and apoptosis in vitro and in vivo
PCA3	PCA3, DD3, NCRNA00019, PCAT3	50652	ENSG00000225937	NR_015342	GRCh38_9:76691980-76863307	prostate cancer	C61.9	NA	qPCR etc.	cell line (LNCaP)	down-regulated	we characterized the expression patterns of several cancer-related genes, including those involved in epithelial-mesenchymal transition (EMT) and AR cofactors in response to PCA3 silencing. We also aimed to develop a strategy to stably silence PCA3. Small interfering RNA (siRNA) or short hairpin RNA (shRNA) was used to knock down PCA3 in LNCaP cells. The expression of 84 cancer-related genes, as well as those coding for AR cofactors and EMT markers, was analyzed by quantitative real-time PCR (qRT-PCR). LNCaP-PCA3 silenced cells differentially expressed 16 of the 84 cancer genes tested, mainly those involved in gene expression control and cell signaling. PCA3 knockdown also induced the upregulation of several transcripts coding for AR cofactors and modulated the expression of EMT markers.	26960690	2016	PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells
PCA3	PCA3, DD3, NCRNA00019, PCAT3	50652	ENSG00000225937	NR_015342	GRCh38_9:76691980-76863307	prostate cancer	C61.9	NA	Northern blot etc.	prostate cancer tissues	up-regulated	Differential display code 3 (DD3(PCA3)) is a novel gene with characteristics that indicate its potentially valuable role in early identification of malignancy and in the construction of interventions directed specifically toward malignantly transformed cells. DD3(PCA3) has a messenger RNA product that is highly overexpressed in tumors. Compared with other genetic markers that are associated with prostate tissue, DD3(PCA3) is the most specific marker for malignant disease.	14607216	2003	New targets for therapy in prostate cancer: differential display code 3 (DD3(PCA3)), a highly prostate cancer-specific gene.
PCAT5	PCAT5, LINC01452, TPCAT-10-36067	102578074	ENSG00000280719	NR_110138	GRCh38_10:35778302-35800920	prostate cancer	C61.9	NA	RNA-seq, qPCR, RNAi etc.	cell lines (PC-3, 22Rv1)	up-regulated	In vitro validation of these alterations revealed a complex integrated phenotype affecting cell growth, migration, invasion, colony-forming potential and apoptosis. Our findings reveal a key molecular determinant of differences between PC and CRPC at the level of the transcriptome. Further, they establish PCAT5 as a novel oncogenic lncRNA in ERG-positive prostate cancers, with implications for defining CRPC biomarkers and new therapeutic interventions.	26282172	2015	Transcriptome sequencing reveals PCAT5 as a novel ERG-regulated long non-coding RNA in prostate cancer.
PCAT6	PCAT6, KDM5B-AS1, KDM5BAS1, PCAN-R1, ncRNA-a2, onco-lncRNA-96	100506696	ENSG00000228288	NR_046325	GRCh38_1:202810954-202812156	non small cell lung cancer	C34	M8046/3	qPCR etc.	NSCLC tissues	up-regulated	To identify lncRNAs that are critical to lung carcinogenesis, we selected three lncRNAs, CAR intergenic 10 (hereafter, CAR10), AK311218, and RP11-480I12.3, from the most up-regulated lncRNAs in the HPR NSCLCs (Table S3) and tested their expression by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The expression of these lncRNAs was consistent with the microarray analysis.	27322209	2016	Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis.
PCGEM1	PCGEM1, LINC00071, NCRNA00071, PCAT9	64002	ENSG00000227418	NR_002769	GRCh38_2:192749845-192776899	prostate cancer	C61.9	NA	qPCR etc.	cell line (LNCaP)	up-regulated	Here, we report a novel function of PCGEM1 that provides growth advantages for prostate cancer cells by regulating tumor metabolism via c-Myc activation. PCGEM1 binds directly to target promoters, physically interacts with c-Myc, promotes chromatin recruitment of c-Myc, and enhances its transactivation activity. We also identified a c-Myc binding domain on PCGEM1 that contributes to the PCGEM1-dependent c-Myc activation and target induction.	25512540	2014	A long noncoding RNA connects c-Myc to tumor metabolism.
PCGEM1	PCGEM1, LINC00071, NCRNA00071, PCAT9	64002	ENSG00000227418	NR_002769	GRCh38_2:192749845-192776899	prostate cancer	C61.9	NA	qPCR etc.	prostate cancer tissues	up-regulated	Expression profiles of genes in CRPC support a role for the transcriptional activity of the PCGEM1.	20868494	2010	LNCaP Atlas: gene expression associated with in vivo progression to castration-recurrent prostate cancer.
PCGEM1	PCGEM1, LINC00071, NCRNA00071, PCAT9	64002	ENSG00000227418	NR_002769	GRCh38_2:192749845-192776899	prostate cancer	C61.9	NA	RNA-seq, qPCR etc.	primary prostate cancer tissues, cell lines (LNCaP, 22RV1, VCaP)	up-regulated	RNA sequencing of two distinct androgen-dependent models shows PCGEM1 to be considerably expressed, while PRNCR1 showed scant basal expression. PCGEM1 was sharply down-regulated following castration and up-regulated upon AR activation in vivo. A PCGEM1-associated gene expression signature (PES) was significantly repressed in response to androgen ablation therapy and in hormone-refractory versus hormone-nave PCa patients. Furthermore, we found PCGEM1 was uniformly distributed in PCa cell nucleus and cytoplasm which remained unaltered upon AR transcriptional activation. PCGEM1 was up-regulated in primary PCa but not in metastasized PCa. 	25744782	2015	The long non-coding RNA PCGEM1 is regulated by androgen receptor activity in vivo.
PCGEM1	PCGEM1, LINC00071, NCRNA00071, PCAT9	64002	ENSG00000227418	NR_002769	GRCh38_2:192749845-192776899	prostate cancer	C61.9	NA	qPCR, RIP etc.	prostate cancer tissues,cell lines (LNCaP, LNCaP-cds1, LNCaP-cds2, CWR22Rv1 etc.), tissues (prostate tumour tissues)	up-regulated	Here we report that two lncRNAs highly overexpressed in aggressive prostate cancer, PRNCR1 (also known as PCAT8) and PCGEM1, bind successively to the androgen receptor and strongly enhance both ligand-dependent and ligand-independent androgen-receptor-mediated gene activation programs and proliferation in prostate cancer cells.	23945587	2013	lncRNA-dependent mechanisms of androgen-receptor-regulated gene activation programs.
POU5F1P1	POU5F1B, OCT4-PG1, OCT4PG1, OTF3C, OTF3P1, POU5F1P1, POU5F1P4, POU5FLC20, POU5FLC8	5462	ENSG00000212993	NA	GRCh38_8:127322183-127420066	prostate cancer	C61.9	NA	qPCR etc.	prostate cancer tissues	up-regulated	POU5F1P1 was found to be the only member of the POU5F1 family to be expressed in prostate with over-expression in prostatic carcinoma compared to surrounding prostatic tissue probably because of an increased density of expressing cells. The probability of a positive repeat biopsy increases with rising PCA3 scores. The PCA3 score was superior to %fPSA for predicting repeat prostate biopsy outcome and may be indicative of clinical stage and significance of pCa.	20017164	2010	POU5F1P1, a putative cancer susceptibility gene, is overexpressed in prostatic carcinoma.
PRNCR1	PRNCR1, CARLo-3, PCAT8	101867536	ENSG00000282961	NR_109833	GRCh38_8:127079874-127092600	prostate cancer	C61.9	NA	qPCR, RIP etc.	prostate cancer tissues, cell lines (LNCaP, LNCaP-cds1, LNCaP-cds2, CWR22Rv1 etc.)	up-regulated	Here we report that two lncRNAs highly overexpressed in aggressive prostate cancer, PRNCR1 (also known as PCAT8) and PCGEM1, bind successively to the androgen receptor and strongly enhance both ligand-dependent and ligand-independent androgen-receptor-mediated gene activation programs and proliferation in prostate cancer cells.	23945587	2013	lncRNA-dependent mechanisms of androgen-receptor-regulated gene activation programs.
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	hepatocellular carcinoma	C22.0	M8170/3	RNAi, Microarray etc.	hepatocarcinoma tissue	down-regulated	We speculated that PVT1 might play a significant role in HCC development and progression via regulation of various pathways and genes, especially DLC1 and the Hippo signaling pathway.Exploring the relationship between DLC1 expression and patient survival, we observed that high DLC1 expression correlated with better survival (51.45±3.93 months) compared to the low DLC1 expression group (45.42±4.23 months, P=0.253, Figure 9C) in HCC. More importantly, due to their wide distribution in the nucleus, lncRNAs can regulate the transcription of adjacent genes by combining the transcription factors or polymerases. 	28979669	2017	Comprehensive analysis of long non-coding RNA PVT1 gene interaction regulatory network in hepatocellular carcinoma using gene microarray and bioinformatics
PVT1	PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100	5820	ENSG00000249859	NR_003367	GRCh38_8:127794533-128101253	gastric cancer	C16	NA	qPCR, Western blot, RIP, ChIP, Luciferase reporter assay etc.	cell lines (AGS, HGC27, NCI-N87, MKN45, MGC803, HEK-293T)	up-regulated	The lncRNA PVT1 was significantly upregulated in gastric cancer tissues compared with ANTs. High expression of PVT1 predicted poor prognosis in patients with gastric cancer. PVT1 enhanced gastric cancer cell proliferation and invasion in vitro and in vivoPVT1 directly bound FOXM1 protein and increased FOXM1 posttranslationally. Moreover, PVT1 is also a FOXM1-responsive lncRNA, and FOXM1 directly binds to the PVT1 promoter to activate its transcription. Finally, PVT1 fulfilled its oncogenic functions in a FOXM1-mediated manner.	27756785	2017	A Positive Feedback Loop of lncRNA-PVT1 and FOXM1 Facilitates Gastric Cancer Growth and Invasion.
SNHG1	SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16	23642	ENSG00000255717	NR_003098	GRCh38_11:62851988-62855914	colorectal cancer	C19.9	NA	qPCR, Western blot	colorectal cancer tissues, cell lines (CCC-HIE-2,SW480, HCT116, HT-29, LOVO, CaCO-2)	up-regulated	SNHG1 expression levels were upregulated aberrantly in colorectal cancer tissues and colorectal cancer cell lines. patients with high SNHG1 expression level had poorer overall survival (OS) and progression-free survival (PFS) than those with low SNHG1 expression.increased SNHG1 expression was proved to be an independent unfavorable prognostic indicator for CRC.SNHG1 silencing inhibited the growth and metastasis and induced apoptosis of CRC cell lines.SNHG1 may induce the activation of the WNT/B-catenin pathway through regulating B-catenin expression and transcription factor-4 (TCF-4), cyclin D1 and MMP-9.	29340086	2017	Up-regulation of lncRNA SNHG1 indicates poor prognosis and promotes cell proliferation and metastasis of colorectal cancer by activation of the Wnt/B-catenin signaling pathway.
SNHG15	SNHG15, C7orf40, Linc-Myo1g, MYO1GUT	285958	ENSG00000232956	NR_003697	GRCh38_7:44983023-44986961	colon cancer	C18	NA	RNA-seq, qPCR etc.	cell lines (HEK-293T, SW1116, HCT116, SW480, and SW620)	down-regulated	Slug is a fast-turnover transcription factor critical for controlling cell fate and cancer cell invasion and metastasis. LncRNA SNHG15 transcription is upregulated in a variety of human cancers according to The Cancer Genome Atlas. Ectopic expression of SNHG15 promoted colon cancer cell migration in vitro, accelerated xenografted tumor growth in vivo, and elevated levels of SNHG15 were associated with poor prognosis for colon cancer patients. Mechanistically, SNHG15 maintains Slug stability in living cells by impeding its ubiquitination and degradation through interaction with the zinc finger domain of Slug. 	29604394	2018	Long non-coding RNA SNHG15 interacts with and stabilizes transcription factor Slug and promotes colon cancer progression.
SNHG16	SNHG16, Nbla10727, Nbla12061, ncRAN	100507246	ENSG00000163597	NR_038108	GRCh38_17:76557766-76565348	colorectal cancer	C19.9	NA	RNA-seq, microarray, qPCR, RNAi etc.	CRC tissues, cell line (HCT116)	up-regulated	SNHG16 is significantly up-regulated in adenomas and all stages of CRC. SNHG16 expression was positively correlated to the expression of Wnt-regulated transcription factors, including ASCL2, ETS2, and c-Myc. In vitro abrogation of Wnt signaling in CRC cells reduced the expression of SNHG16 indicating that SNHG16 is regulated by the Wnt pathway. Silencing of SNHG16 resulted in reduced viability, increased apoptotic cell death and impaired cell migration. The SNHG16 silencing particularly affected expression of genes involved in lipid metabolism. A connection between SNHG16 and genes involved in lipid metabolism was also observed in clinical tumors.	27396952	2016	SNHG16 is regulated by the Wnt pathway in colorectal cancer and affects genes involved in lipid metabolism.
SNHG20	SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG	654434	ENSG00000234912	NR_027058	GRCh38_17:77086716-77094990	gastric cancer	C16	NA	qPCR, Western blot, RIP etc.	gastric cancer cell lines (Bgastric cancer823, Sgastric cancer-7901, MKN45), hepatocarcinoma tissues	up-regulated	Thus, the results showed that SNHG20 acted as an oncogene in GC and targeting SNHG20 may serve as a therapeutic target for GC. The western-blotting results showed that knockdown of SNHG20 significantly inhibited the expression levels of transcription factor Twist1 and EMT maker Vimentin, but upregulating the E-cadherin expression in MKN45 cells.LncRNAs could regulated cancer cells phenotypes through regulating target gene expression by different mechanisms, including chromatin modification, genomic imprinting, RNA decay and sponging miRNAs [20]. 	29113337	2017	Long noncoding RNA SNHG20 promotes gastric cancer progression by inhibiting p21 expression and regulating the GSK-3B/ B-catenin signaling pathway.
SPRY4-IT1	SPRY4-IT1, SPRIGHTLY	100642175	ENSG00000281881	NR_131221	NA	esophageal squamous cell cancer	NA	NA	qPCR, Western blot, Cell proliferation assay etc.	cell lines (Eca109, KYSE150, Eca9706, EC18, EC1 etc.)	up-regulated	We find that the expression of lncRNA SPRY4-IT1 is significantly upregulated in ESCC cell lines as compared with human esophageal epithelial cell line HEEC. Overexpression of SPRY4-IT1 can increase in vitro motility of ESCC cells via induction of epithelial-mesenchymal transition (EMT), which is characterized by increasing the expression of vimentin (Vim) and fibronectin (FN) with a concomitant decrease of E-cadherin (E-Cad) and ZO-1. Further, the knockdown of SPRY4-IT1 also significantly attenuates TFG-B-induced EMT of ESCC cells. Further, 	27250657	2016	Upregulation of long noncoding RNA SPRY4-IT1 promotes metastasis of esophageal squamous cell carcinoma via induction of epithelial-mesenchymal transition.
TCONS_l2_00022545	NA	NA	NA	NA	NA	colorectal cancer	C19.9	NA	qPCR, RNAi etc.	CRC tissues	up-regulated	Results showed that knockdown of LOC100190940 and TCONS_l2_00022545 significantly downregulated their neighboring protein-coding genes. Additionally, knockdown of the two lncRNAs significantly decreased cell proliferation and migration.	27004403	2016	Integrated analysis of long non-coding RNAs in human colorectal cancer.
TRERNA1	TRERNA1, LINC00651, treRNA	100887755	ENSG00000231265	NR_051976	GRCh38_20:50040716-50041504	gastric cancer	C16	NA	qPCR, Western blot, RIP etc.	gastric cancer tissues, gastric cancer cell lines (MKN-28, MKN-45, Bgastric cancer-823, AGS, Mgastric cancer-803)	up-regulated	In the present study, we demonstrate that lncRNA TRERNA1 acts like an enhancer of SNAI1 to promote cell invasion and migration and to contribute to metastasis of gastric cancer (GC).  Further studies have shown that TRERNA1 not just inhibits the expression of CDH1 by enhancing SNAI1 expression, but also epigenetically silenced CDH1 by recruiting EZH2 to carry out histone methylation of its promoter region. lncRNA TRERNA1 was identified and located close to SNAI1, which is an epithelial-mesenchymal transition (EMT) master regulator transcription factor.It has been found that the expression of CDH1 is not only regulated by the transcription factor SNAI1, but also by epigenetic modification, such as microRNA (miRNA), DNA methylation, and histone modification.	28918030	2017	LncRNA TRERNA1 Function as an Enhancer of SNAI1 Promotes Gastric Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition.
TUG1	TUG1, LINC00080, NCRNA00080, TI-227H	55000	ENSG00000253352	NR_002323	GRCh38_22:30969245-30979395	hepatocellular carcinoma	C22.0	M8170/3	qPCR, RNAi, Western blot, RIP, Flow cytometry assay etc.	HCC tissues, cell lines (HepG2, MHCC-97H, Hep3B etc.)	up-regulated	TUG1 expression was up-regulated in HCC tissues and the higher expression of TUG1 was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. Moreover, silencing of TUG1 expression inhibited HCC cell proliferation, colony formation, tumorigenicity and induced apoptosis in HCC cell lines. We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region.	26336870	2015	Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2.
UCA1	UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36	652995	ENSG00000214049	NR_015379	GRCh38_19:15828206-15836326	bladder cancer	C67	NA	qPCR, RNAi, Luciferase reporter assay etc.	cell lines (5637, T24, BLZ-211, BLS-211)	up-regulated	In the present study, we showed that lncRNA-UCA1 expression in bladder cancer cells was upregulated by transcription factor CCAAT/enhancer binding protein a (C/EBPa), The transcriptional activation of lncRNA-UCA1 by C/EBPa also contributes to the increased viability and decreased apoptosis of bladder cancer cells.	24648007	2014	Upregulation of long non-coding RNA urothelial carcinoma associated 1 by CCAAT/enhancer binding protein a contributes to bladder cancer cell growth and reduced apoptosis.
UCA1	UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36	652995	ENSG00000214049	NR_015379	GRCh38_19:15828206-15836326	bladder cancer	C67	NA	qPCR, Western blot, ChIP, Luciferase reporter assay etc.	cell lines (BLZ-211 and BLS-211)	differential expression	To verify if Ets-2 induced UCA1 gene expression was involved in apoptosis we studied another bladder TCC cell line, called BLS-211. BLS-211 is lack of endogenous UCA1 expression and is derived from the same patient as BLZ-211 cell line. Interestingly, after knocking down the Ets-2 gene, we didn’t observed subsequent apoptosis in BLS-211 cells. Additionally, we counted the apoptotic cells using flow cytometry in both cell lines separately. Consistent with the fluorescence microscope results, the flow cytometry results revealed a significant increase of cell pro-apoptosis (upper right quadrant) after Ets-2 knockdown in BLZ-211 cells while no increase of pro-apoptosis was observed after Ets-2 knockdown in BLS-211 cells. These results suggested that UCA1 may be involved in the cell apoptosis induced by the suppression of the Ets-2.	24069250	2013	Ets-2 regulates cell apoptosis via the Akt pathway, through the regulation of urothelial cancer associated 1, a long non-coding RNA, in bladder cancer cells.