Journal Article

miR-106b downregulates adenomatous polyposis coli and promotes cell proliferation in human hepatocellular carcinoma

Gang Shen, Hongyun Jia, Qiang Tai, Yanhao Li and Deji Chen

in Carcinogenesis

Volume 34, issue 1, pages 211-219
Published in print January 2013 | ISSN: 0143-3334
Published online October 2012 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgs320
miR-106b downregulates adenomatous polyposis coli and promotes cell proliferation in human hepatocellular carcinoma

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Aberrant activation of the Wnt/β-catenin signal pathway is frequently observed in hepatocellular carcinoma (HCC). β-Catenin is the major cellular effector of Wnt signaling and inactivation of adenomatous polyposis coli (APC) results in nuclear accumulation of β-catenin. Therefore, it was speculated that APC inhibition could play important roles in activating the Wnt/β-catenin pathway and in HCC progression. In this study, we report that miR-106b expression is markedly upregulated in hepatoma cells and hepatoma tissues compared with immortalized normal liver epithelial cells and normal hepatic tissues. Ectopic expression of miR-106b induces the proliferation and anchorage-independent growth of hepatoma cells, whereas inhibition of miR-106b reduced this effect. Furthermore, miR-106b upregulation in hepatoma cells modulated entry into the G1/S transitional phase by upregulating cyclin D1 and downregulating APC. Moreover, we demonstrated that miR-106b downregulates APC expression by directly targeting the 3′-untranslated region of APC messenger RNA. Taken together, our results suggest that miR-106b plays an important role in promoting the proliferation of human hepatoma cells and presents a novel mechanism of micro RNA-mediated direct suppression of APC expression in cancer cells.

Journal Article.  5301 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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