HCV NS5A interacts with p53 and inhibits p53-mediated apoptosis

摘要: Hepatitis C virus (HCV) causes a persistent infection, chronic hepatitis and hepatocellular carcinoma. HCV NS5A, one of non-structural proteins HCV, was suggested to play role in oncogenic transformation. Since the tumor suppressor p53 is important for preventing neoplastic transformation, we investigated functional effects NS5A on p53. In vitro vivo coimmunoprecipitation confocal microscopy were used determine interaction binds directly colocalizes perinuclear region. inhibits transcriptional transactivation by dose-dependent manner use reporter assay. Down regulation endogenous p21/waf1 expression, which activated Hep3B cells, demonstrated using FLAG- FLAG-NS5A stable cell lines. The effect p53-mediated apoptosis determined flow cytometry both permanently transiently transfected cells with exogenous p53-induced abrogated inhibition correlates well binding ability addition, protein interacts hTAF(II)32, component TFIID an essential coactivator p53, vivo. These results suggest that partially sequestrates hTAF(II)32 cytoplasm suppresses during may contribute hepatocarcinogenesis infection.