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miR-511 promotes the proliferation of human hepatoma cells by targeting the 3'UTR of B cell translocation gene 1 (BTG1) mRNA

         

摘要

Aberrant expression of miR-511 is involved in the development of cancer,but the role of miR-511 in hepatocellular carcinoma (HCC) is not well documented.In this study,we explored the molecular mechanisms of miR-511 in hepatocarcinogenesis.Our results of bioinformatics analysis suggested that B cell translocation gene 1 (BTG1),a member of anti-proliferative gene family,was one of the putative targets of miR-511.The expression levels of miR-511 were significantly higher in 30 clinical HCC tissues than in corresponding peritumor tissues,and were negatively correlated with those of BTG1 in the HCC tissues (r=-0.6105,P<O.01).In human hepatoma cell lines HepG2 and H7402,overexpression of miR-511 dose-dependently inhibited the expression of BTG1,whereas knockdown of miR-511 dose-dependently increased the expression of BTG1.Luciferase reporter gene assays verified that miR-511 targeted the 3'UTR of BTG1 mRNA.In the hepatoma cells,overexpression of miR-511 significantly decreased BTG1-induced G1 phase arrest,which was rescued by overexpression of BTG1.Furthermore,overexpression of miR-511 promoted the proliferation of the hepatoma cells,which was rescued by overexpression of BTG1.Conversely,knockdown of miR-511 inhibited cell proliferation,which was reversed by knockdown of BTG1.In conclusion,miR-511 promotes the proliferation of human hepatoma cells in vitro by targeting the 3'UTR of BTG1 mRNA.

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  • 来源
    《中国药理学报:英文版》 |2017年第8期|1161-1170|共10页
  • 作者单位

    State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China;

    Department of Hepatology, The First Hospital, Jilin University, Changchun 130021, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Biochemistry, College of Life Sciences,Nankai University, Tianjin 300071, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Cancer Research, College of Life Sciences, Nankai University, Tianjin 300071, China;

    State Key Laboratory of Medicinal Chemical Biology, Department of Biochemistry, College of Life Sciences,Nankai University, Tianjin 300071, China;

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