國家衛生研究院 NHRI:Item 3990099045/2761
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    题名: Hepatitis B virus X protein inhibits transforming growth factor-beta-induced apoptosis through the activation of phosphatidylinositol 3-kinase pathway
    作者: Shih, WL;Kuo, ML;Chuang, SE;Cheng, AL;Doong, SL
    贡献者: National Institute of Cancer Research
    摘要: Transforming growth factor-beta (TGF-beta) is a potent inducer of apoptosis in Hep 3B cells. This work investigated how hepatitis B virus X protein (HBx) affects TGF-beta-induced apoptosis. Trypan blue exclusion and colony formation assays revealed that HBx increased the ID50 toward TGF-beta. In the presence of HBx, TGF-beta-induced DNA laddering was decreased, indicating that HBx had the ability to block TGF-beta-induced apoptosis. Furthermore, HBx did not alter the expression levels of type I and type II TGF-beta receptors. HBx did not affect TGF-beta-induced activation of promoter activities of the plasminogen activator inhibitor-1 (PAI-I) gene. These results indicate that HBx interferes with only a subset of TGF-beta activity. In the presence of phosphatidylinositol (PI) 3-kinase inhibitors, wortmannin or LY294002, the HBx-mediated inhibitory effect on TGF-beta-induced apoptosis was alleviated. In addition, the tyrosine phosphorylation levels of the regulatory subunit p85 of phosphatidylinositol 3-kinase (PI 3-kinase) and PI 3-kinase activity were elevated in stable clones with HBx expression. Transactivation-deficient mutants of HBx lost their ability to inhibit TGF-beta-induced apoptosis. Phosphorylation of the p85 subunit of PI 3-kinase and Akt, a downstream target of PI 3-kinase, was not observed in stable clones with transactivation-deficient HBx mutant's expression. Thus, the anti-apoptotic effect of HBx against TGF-beta can be mediated through the activation of the PI 3-kinase signaling pathway, and the transactivation function of HBx is required for its anti-apoptosis activity.
    关键词: Biochemistry & Molecular Biology
    日期: 2000-08-18
    關聯: Journal of Biological Chemistry. 2000 Aug;275(33):25858-25864.
    Link to: http://dx.doi.org/10.1074/jbc.M003578200
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1083-351X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000088849400104
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0034682769
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