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. 2013 Feb;29(2):653-61.
doi: 10.3892/or.2012.2138. Epub 2012 Nov 14.

Inhibition of miR-96 expression reduces cell proliferation and clonogenicity of HepG2 hepatoma cells

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Inhibition of miR-96 expression reduces cell proliferation and clonogenicity of HepG2 hepatoma cells

Dong Xu et al. Oncol Rep. 2013 Feb.

Abstract

microRNAs (miRNAs) are negative regulators of gene expression and can function as tumor suppressors or oncogenes. Several miRNAs are associated with the development of hepatocellular carcinoma (HCC). miR-96 has been closely associated with cell proliferation and clonogenicity. Upregulation of miR-96 has been observed in various types of cancer. However, the biological function of miR-96 in hepatocarcinogenesis remains largely unknown. In this study, we demonstrated that miR-96 was upregulated in HCC and inhibition of miR-96 significantly suppressed HCC cell proliferation and colony formation. The expression levels of forkhead box O1 (FOXO1) and forkhead box O3a (FOXO3a) were upregulated when miR-96 was inhibited in HCC cells and the inhibition of FOXO1 and FOXO3a promoted HCC cell proliferation and colony formation. Collectively, these data reveal an important contribution of miR-96 to hepatocarcinogenesis and suggest a role for FOXO1 and FOXO3a dysregulation in this process. Thus, the use of a synthetic inhibitor of miR-96 may be a promising approach for the treatment of HCC.

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