Article ID Journal Published Year Pages File Type
2130169 Experimental Cell Research 2015 10 Pages PDF
Abstract

•miR-208-3p was highly expressed and directly repressed the expression of ARID2 in HCC.•miR-208-3p contributed to HCC cell progression both in vitro and in vivo.•Over-expression of ARID2 inhibited the HCC cell proliferation and invasion.•Restoration of ARID2 partly reversed the the effect of miR-208-3p down-regulation on HCC cells.•Newly regulatory pathway: miR-208-3p mediated the repression of ARID2 by TGFβ1 in HCC cells.

MicroRNAs (miRNAs) are small non-coding RNAs that negatively regulate gene expression at post-transcriptional level. miRNA dysregulation plays a causal role in cancer progression. In this study, miR-208-3p was highly expressed and directly repressed ARID2 expression. As a result, ARID2 expression in hepatocellular carcinoma (HCC) was decreased. In vitro, miR-208-3p down-regulation and ARID2 over-expression elicited similar inhibitory effects on HCC cell proliferation and invasion. In vivo test results revealed that miR-208-3p down-regulation inhibited HCC tumorigenesis in Hep3B cells. Moreover, ARID2 was possibly a downstream element of transforming growth factor beta1 (TGFβ1)/miR-208-3p/ARID2 regulatory pathway. These findings suggested that miR-208-3p up-regulation is associated with HCC cell progression and may provide a new target for liver cancer treatment.

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Life Sciences Biochemistry, Genetics and Molecular Biology Cancer Research
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