Downregulation of miR‐7 upregulates Cullin 5 (CUL5) to facilitate G1/S transition in human hepatocellular carcinoma cells. Issue 12 (13th December 2013)

• Record Type: Journal Article
• Authors: Ma, Chaoqun; Qi, Ying; Shao, Liping; Liu, Min; Li, Xin; Tang, Hua
• Is Part Of: IUBMB life. Volume 65:Issue 12(2013:Dec.)
• Page Start: 1026
• Page End: 1034
• Publication Date: 2013-12-13
• Subjects: Biochemistry -- Periodicals; Molecular biology -- Periodicals; 572.8
• DOI: 10.1002/iub.1231
• Languages: English
• ISSNs: 1521-6543

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <p>MicroRNAs (miRNAs) are small, non‐coding RNAs that participate in the regulation of gene expression. In this study, we demonstrate that miR‐7 was downregulated in hepatocellular carcinoma (HCC) tissues compared to adjacent non‐tumor tissue. Over‐expression of miR‐7 in QGY‐7703 and HepG2 cell lines inhibited colony formation and induced G1/S phase arrest, whereas knockdown of miR‐7 produced the opposite phenotype. A tumor suppressor gene, CUL5, was identified as a direct target of miR‐7, and CUL‐5 is upregulated upon the binding of miR‐7 to its 3′UTR. Furthermore, suppression of CUL5 also suppressed cell colony formation and induced cell cycle arrest. Ectopic expression of CUL5 abrogated the effects of miR‐7 inhibition on QGY‐7703 and HepG2 cell lines. These results indicate that miR‐7 suppresses colony formation and causes cell cycle arrest via upregulation of CUL5, and it may function as a tumor suppressor in HCC. © 2013 IUBMB Life, 65(12):1026–1034, 2013</p> </abstract>