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miR-126 inhibits cell proliferation and induces cell apoptosis of hepatocellular carcinoma cells partially by targeting Sox2

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Abstract

Hepatocellular carcinoma (HCC) is the fifth most common malignancy and the third leading cause of cancer-related death globally. MicroRNAs (miRNAs) represent a new cohort of gene regulators. Currently, a large number of miRNAs have been reported to be associated with the initiation and maintenance of HCC. Through evaluating the relative concentrations of HCC-associated circulating miRNAs, underexpression of miR-126 has been identified in the blood of HCC patients. However, the exact function of miR-126 on HCC cellular biology progression and relative mechanisms were unclear. In this paper, we explored the function of miR-126 on HCC cells through exogenously transfecting HCC cells with miR-126 mimic. Restored miR-126 expression inhibited cell proliferation, arrest cell cycle progression, and induced cell apoptosis of HepG2 HCC cells. Moreover, to explore the mechanism of miR-126-mediated tumor suppression, we searched the putative targets of miR-126 using prediction program. Surprisingly, we found that sex-determining region Y-box 2 (Sox2) was a putative target gene of miR-126. Further luciferase assays, mRNA and protein assays consistently validated the target role of Sox2. Through restoring the expression of Sox2 in miR-126-transfected HepG2 cells, we found that overexpression of Sox2 could partially abrogate the miR-126-mediated suppression of cell growth. Thus, our data identified miR-126 as a tumor suppressor in HCC through, at least partially by targeting Sox2. This may provide novel diagnostic and therapeutic options for human HCC in future.

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Acknowledgments

This work was supported by national natural science foundation of China (No. 81101693).

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Correspondence to Li Chang.

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Zhao, C., Li, Y., Zhang, M. et al. miR-126 inhibits cell proliferation and induces cell apoptosis of hepatocellular carcinoma cells partially by targeting Sox2 . Human Cell 28, 91–99 (2015). https://doi.org/10.1007/s13577-014-0105-z

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