4.7 Article

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

Journal

CANCER LETTERS
Volume 382, Issue 2, Pages 166-175

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2016.08.029

Keywords

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

Categories

Funding

  1. National Natural Science Foundation of China [91029714, 31270818, 81572790, 31301132]
  2. Natural Science Foundation of Tianjin [12JCZDJC25100, 16JCQNJC10500]
  3. Natural Sciences Foundation of Tianjin Medical University [2014KYQ19]

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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. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

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