Microrna-342 inhibits hepatocellular carcinoma cell proliferation and promotes apoptosis through the FOXP1/MYCBP Signaling Axis

Microrna-342通过FOXP1/MYCBP信号轴抑制肝细胞癌细胞增殖并促进细胞凋亡

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Abstract

To investigate the role and mechanism of miR-342 and FOXP1 on hepatocellular carcinoma cells. QRT-PCR was applied to determine the expression of miR-342, FOXP1 and MYCBP in normal hepatocyte cell lines (NHC), hepatocellular carcinoma cell lines (HEK-293 T) and human hepatocellular carcinoma cell lines (HepG2, MHCC97-L, Huh7 and SMMC7721). After knockdown or over-expression of miR-342 and FOXP1 in HepG2 cells respectively, cell proliferation and cell viability were measured using MTT assay and colony formation assay. Flow cytometry was adopted to test for apoptosis. Dual luciferase gene reporter assays were performed to validate the target relationship between FOXP1and miR-342 or MYCBP. The level of apoptosis-related proteins cleaved-caspase-3, Bcl-2 and Bax were measured by western blot. Compared with NHC, miR-342 expression was decreased and FOXP1 expression was up-regulated in hepatocellular carcinoma cell lines. MiR-342 could target and negatively regulate FOXP1. FOXP1 could promote the proliferation of hepatocellular carcinoma cells, positively regulate the expression of c-Caspase-3, Bax, negatively regulate Bcl-2 and inhibit apoptosis. FOXP1 can also target and positively regulate MYCBP. The expression of MYCBP was up-regulated in the hepatocellular carcinoma cell lines, while overexpression of miR-342 decreased MYCBP expression promoted by overexpression of FOXP1. MiR-342 can inhibit FOXP1/MYCBP signaling axis to regulate the members of Caspase-3 and Bcl-2 family to inhibit the proliferation and promote apoptosis of hepatocellular carcinoma cells.

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