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Table 3 LncRNAs with an epigenetic function in cancer

From: Long non-coding RNAs regulate drug resistance in cancer

NameCancerMechanismRef.
ecCEBPAUpregulated in gastric cancer; inverse correlation with CEBPA in leukaemia cell lines.association with DNMT1 regulates DNA methylation[106,107,108]
XistAbnormal expression in hematologic cancer. influences X reactivation and results in genome-wide changes; directly interacts with SHARP to silence transcription through HDAC3; binds PRC2(the epigenetic complex responsible for trimethylation of histone H3 lysine 27 methylation), and targets PRC2 to Xi;[109,110,111]
HOTAIRUpregulated in epithelial cancer cells, such as primary breast tumors and metastases, gastric cancer, oral squamous cell carcinoma glioblastoma multiforme, colorectal cancer, esophageal squamous cell carcinoma etc., and promotes cancer metastasis. Induces genome-wide re-targeting of PRC2 to an occupancy pattern, leading to altered histone H3 lysine 27 methylation, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. HOTAIR promotes EMT by switching histone H3 lysine 27 acetylation to methylation at the E cadherin promoter, which induces the transcriptional inhibition of E cadherin. interacts with PRC2 and LSD1 complex, and as a histone scaffold, to inhibit the transcription of the HOXD cluster[112,113,114,115,116,117]
H19Upregulated in different cancer types, such as colorectal cancer, breast cancer, ovarian cancer cells, etc., and promotes oncogenesis and drug resistance. Interacts with SAHH to regulate the DNMT3B - dependent DNA methylation at different genetic loci. The impact of H19 on metastasis could be due to the sequestration of different microRNAs[12, 118,119,120,121]
MITA1A new identified energy stress-inducible lncRNA that promotes hepatocellular carcinoma metastasisMITA1 may regulate the transcription of Slug to promote the epithelial-mesenchymal transition[122]
TARIDDeregulated in various human cancersRecruits the DNA demethylation regulator, GADD45α, to activate the transcription of the tumor suppressor gene, TCF21.
GADD45A is an epigenetic R-loop reader that recruits the demethylation machinery to promoter CGIs.
[123, 124]
MALAT1Upregulated in lung cancer, gastric cancer, colorectal cancer, hepatocellular carcinoma, thoracic aortic aneurysm;
Deregulated in breast cancer
Oct4 transcriptionally activates MALAT1 via enhancer binding to promote cell proliferation and motility, causing lung tumorigenesis and poor prognosis. MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p in GC cells. the rs664589 G allele alters the binding of MALAT1 to miR-194-5p, resulting in increased expression of MALAT1 in colorectal cancer; MALAT1 regulates cancer glucose metabolism, enhancing glycolysis, and inhibiting gluconeogenesis via elevated translation of the transcription factor TCF7L2. MALAT1 binds and inactivates the prometastatic transcription factor TEAD, preventing TEAD from associating with its co-activator, YAP, and target gene promoters in breast cancer. interacts with DBC1 to regulate p53 acetylation. The HDAC9-MALAT1-BRG1 complex binds chromatin and represses contractile protein gene expression in association with gain of histone H3-lysine 27 trimethylation modifications.[125,126,127,128,129,130,131]
NEAT1Upregulated in lung cancerOct4 transcriptionally activates NEAT1 via promoter binding to facilitate cell proliferation and motility, causing lung tumorigenesis and poor prognosis.[126]
ANRILHigh expression linked to poor outcome. ANRIL was identified as an oncogene in a number of tumors such as acute myeloid leukemia, gastric cancer, lung cancer, hepatocellular carcinoma, and esophageal squamous cell carcinoma. represses the expression of adiponectin receptor (AdipoR1), which is a key regulator of glucose metabolism, which affects the phosphorylation of AMPK and SIRT1. represses KLF2 transcription by binding to PRC2 and recruiting it to the KLF2 promoter region.[132,133,134,135]
AFAP1-AS1High expression linked to poor outcome in non-small cell lung cancerAFAP1-AS1 interacts with EZH2 and recruits EZH2 to the promoter regions of p21, epigenetically repressing p21 expression.[136]