Open Access

ARTICLE

miR-935 Promotes Liver Cancer Cell Proliferation and Migration by Targeting SOX7

Xiaorui Liu^*†1, Jingjing Li^*1, Zujiang Yu^*, Juan Li^*, Ranran Sun^*, Quancheng Kan^‡

* Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China
† Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China
‡ Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China
1 These authors provided equal contribution to this work.

Oncology Research 2017, 25(3), 427-435. https://doi.org/10.3727/096504016X14747300207374

Abstract

Hepatocellular carcinoma (HCC) is the most common cancer in the world. MicroRNAs (miRNAs) are a type of small noncoding RNA that can regulate the expression of target genes under physiological and pathophysiological conditions. Aberrant expression of microRNA-935 (miR-935) has been reported in cancer studies. However, its expression and mechanism in HCC remain unclear. In our study, we found that miR-935 was upregulated in liver cancer tissues and cells. Overexpression of miR-935 in liver cells promoted cell proliferation, tumorigenesis, and cell cycle progression, whereas inhibition of miR-935 reduced cell proliferation, tumorigenicity, and cell cycle progression. These changes in the properties of HCC cells were associated with upregulation of two well-known cellular G₁/S transitional regulators: cyclin D1 and c-Myc. Additionally, we identified SOX7 as a direct target of miR-935. Overexpression of miR-935 inhibited SOX7 expression but promoted the levels of c-Myc and cyclin D1, which promotes cell proliferation and tumorigenesis; knockdown of miR-935 increased SOX7 level and inhibited c-Myc and cyclin D1 expression, whereas SOX7 silencing could promote cell proliferation, cell motility, and invasiveness in vitro. Our findings suggest that miR-935 represents a biomarker and a potential new target in HCC progression by suppressing SOX7 expression.

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