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  • Title: [Hepatitis B virus X protein induces malignant transformation tendency of Chang liver cells involving p16(INK4a) hypermethylation].
    Author: Lv WP, Zhou KL, Gao B, Chen YL, Xiang X, Su M, Dong JH.
    Journal: Beijing Da Xue Xue Bao Yi Xue Ban; 2012 Dec 18; 44(6):932-6. PubMed ID: 23247461.
    Abstract:
    OBJECTIVE: To study the relationship between hepatitis B virus X (HBx) protein and DNA methylation of p16(INK4a) and the role of HBx in the carcinogenesis of hepatocellular carcinoma. METHODS: Eukaryonic expression vectors pcDNA3.1B-HBx and pcDNA3.1B were transduced into Chang liver cells by using Lipofectamine 2000 to establish the Chang-HBx liver cell line (HBx expression) and Chang-vector liver cell line (non-HBx expression). RT-PCR and Western blot were used to test the expression of p16(INK4a) in the two cell lines. The level of p16(INK4a) promoter methylation was tested by methylation specific PCR (MSP). The proliferation curves were drew by CCK-8, and S-phase in cell cycle and apoptosis were observed by flow cytometry. RESULTS: Hypermethylation of p16 can be mediated by HBx, which decreases the expression of mRNA and protein of p16. Chang-HBx cells grow faster. Chang-HBx cells have much higher S-phase population (28.96% vs. 21.53%, P<0.001; 28.96% vs. 21.5%, P<0.001) and lower apoptosis rate (2.71% vs. 3.69%, P<0.001; 2.71% vs. 3.36%, P<0.001) than Chang-vector cells and Chang cells respectively. CONCLUSION: p16(INK4a) expression was repressed by HBx protein via DNA methylation of p16(INK4a), which can induce the malignant transformation tendency of Chang cells.
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