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

被引:108
|
作者
Lv, Jing
Fan, Hong-xia
Zhao, Xiao-pei
Lv, Ping
Fan, Jing-yi
Zhang, Yi
Liu, Min
Tang, Hua [1 ]
机构
[1] Tianjin Med Univ, Tianjin Life Sci Res Ctr, Tianjin 300070, Peoples R China
基金
中国国家自然科学基金;
关键词
Long non-coding RNA (lncRNA); HCC migration/invasion; lncRNA-Unigene56159; Slug; miR-140-5p; COMPETING ENDOGENOUS RNA; TUMOR-GROWTH; COLORECTAL-CANCER; EXPRESSION; METASTASIS; INVASION; MICRORNAS; PROLIFERATION; TUMORIGENESIS; PROGRESSION;
D O I
10.1016/j.canlet.2016.08.029
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:166 / 175
页数:10
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