Format

Send to

Choose Destination
Cancer Lett. 2016 Nov 28;382(2):166-175. doi: 10.1016/j.canlet.2016.08.029. Epub 2016 Sep 3.

Long non-coding RNA Unigene56159 promotes epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells.

Author information

1
Tianjin Life Science Research Center and Department of Pathology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
2
Tianjin Life Science Research Center and Department of Pathology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China. Electronic address: htang2002@yahoo.com.

Abstract

HBV infection has been reported to be closely associated with HCC development; however, the underlying mechanisms are unclear. Emerging evidence has indicated that long non-coding RNAs (lncRNAs) play important regulatory roles in the pathogenesis and progression of cancers. To investigate the important role and mechanism of lncRNAs in the progression of HBV-related HCC, we screened lncRNAs in HBV-positive and HBV-negative HCC tissues. We identified a novel lncRNA, lncRNA-Unigene56159, which is highly expressed in HBV-related HCC tissues, and further analysis showed that this lncRNA was induced by HBV in vitro. Functionally, Unigene56159 significantly promoted cell migration/invasion and epithelial-mesenchymal transition (EMT) in HCC. Mechanistically, Unigene56159 could directly bind to miR-140-5p and effectively act as a competing endogenous RNA (ceRNA) for miR-140-5p to de-repress the expression of the target gene Slug. Collectively, our findings indicate that the Unigene56159/miR-140-5p/Slug axis contributes to HCC cell migration and invasion, which may provide novel insights into the function of lncRNA-driven hepatocarcinogenesis.

KEYWORDS:

HCC migration/invasion; Long non-coding RNA (lncRNA); Slug; lncRNA-Unigene56159; miR-140-5p

PMID:
27597739
DOI:
10.1016/j.canlet.2016.08.029
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center