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Hepatocellular carcinoma (HCC) is one of the most common malignant cancers. To elucidate new regulatory mechanisms for heptocarcinogenesis, we investigated the regulation of p21, a cyclin-dependent kinase (CDK) inhibitor encoded by  CDKN1A , in HCC. The expression level of p21 is decreased with the progression of HCC. Luciferase assays with a luciferase-p21-3′ UTR reporter and its serial deletions identified a 15-bp repressor element at the 3′-UTR of  CDKN1A , which contains a binding site for  miR-95-3p . Mutation of the binding site eliminated the regulatory effect of  miR-95-3p  on p21 expression. Posttranscriptional regulation of p21 expression by  miR-95-3p  is mainly on the protein level (suppression of translation). Overexpression of  miR-95-3p  in two different HCC cell lines, HepG2 and SMMC7721, significantly promoted cell proliferation, cell cycle progression and cell migration, whereas a  miR-95-3p  specific inhibitor decreased cell proliferation, cell cycle progression and cell migration. The effects of  miR-95-3p  on cellular functions were rescued by overexpression of p21. Overexpression of  miR-95-3p  promoted cell proliferation and tumor growth in HCC xenograft mouse models. Expression of  miR-95-3p  was significantly higher in HCC samples than in adjacent non-cancerous samples. These results demonstrate that  miR-95-3p  is a potential new marker for HCC and regulates hepatocarcinogenesis by directly targeting  CDKN1A /p21 expression.

Up-regulation of miR-95-3p in hepatocellular carcinoma promotes tumorigenesis by targeting p21 expression