LncRNA FOXD2-AS1 plays an oncogenic role in hepatocellular carcinoma through epigenetically silencing CDKN1B(p27) via EZH2.

Accumulating reports suggest that long noncoding RNAs (lncRNAs) play critical roles in the progression of many tumors. In this study, we explored the expression level of lncRNA FOXD2-AS1 in the tumorigenesis of hepatocellular carcinoma (HCC). The data indicated that FOXD2-AS1 expression was increased in HCC specimens and cell lines. Furthermore, aberrant expression was correlated with tumor number and tumor size in HCC patients. Silencing FOXD2-AS1 arrest cell cycle in the G0/G1 phase, inhibited colony formation, cell proliferation and suppressed the in vivo growth of subcutaneous tumors. Our results revealed that FOXD2-AS1 could epigenetically silence CDKN1B by recruiting EZH2 to CDKN1B promoter region. Knocking down CDKN1B could restore the carcinogenic effect of FOXD2-AS1 on HCC. Collectively, our data suggested that FOXD2-AS1 could be new target for therapies or prognostic biomarker in hepatocellular carcinoma.

Xu K ，Zhang Z ，Qian J ，Wang S ，Yin S ，Xie H ，Zhou L ，Zheng S ... -  《-》

EGR1-induced upregulation of lncRNA FOXD2-AS1 promotes the progression of hepatocellular carcinoma via epigenetically silencing DKK1 and activating Wnt/β-catenin signaling pathway.

Lei T ，Zhu X ，Zhu K ，Jia F ，Li S ... -  《-》

LncRNA LEF1-AS1 silencing diminishes EZH2 expression to delay hepatocellular carcinoma development by impairing CEBPB-interaction with CDCA7.

Gao J ，Dai C ，Yu X ，Yin XB ，Zhou F ... -  《-》

Long noncoding RNA DDX11-AS1 epigenetically represses LATS2 by interacting with EZH2 and DNMT1 in hepatocellular carcinoma.

Long noncoding RNAs (lncRNAs), a group of transcripts without protein coding potential, have been reported to play critical roles in progression of hepatocellular carcinoma (HCC). However, the biological role of DDX11-AS1 in HCC is not clear. In this study, we found that DDX11-AS1 expression was dramatically higher in HCC tissues and cell lines. Higher DDX11-AS1 expression predicted poor overall survival of patients. Functionally, the proliferation, cell cycle progression, migration, and invasion of HCC cells were inhibited by DDX11-AS1 silencing, while promoted by ectopic expression of DDX11-AS1. RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays validated that DDX11-AS1 suppressed LATS2 expression by interacting with EZH2 and DNMT1 in HCC cells. Knockdown of DDX11-AS1 increased the mRNA and protein levels of LATS2. Overexpression of LATS2 abolished the promotive effect of DDX11-AS1 on cell growth and invasion. Besides, DDX11-AS1 promoted tumor formation in vivo. The mRNA levels of LATS2 were markedly decreased in tumor tissues and negatively correlated with DDX11-AS1 expression. Taken together, our data indicated that DDX11-AS1 may be a novel oncogene in hepatocarcinogenesis by repressing LATS2, providing a potential therapeutic target for HCC treatment.

Li Y ，Zhuang W ，Huang M ，Li X ... -  《-》

Upregulation of the long noncoding RNA FOXD2-AS1 promotes carcinogenesis by epigenetically silencing EphB3 through EZH2 and LSD1, and predicts poor prognosis in gastric cancer.

Xu TP ，Wang WY ，Ma P ，Shuai Y ，Zhao K ，Wang YF ，Li W ，Xia R ，Chen WM ，Zhang EB ，Shu YQ ... -  《-》