國家衛生研究院 NHRI:Item 3990099045/2373
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    題名: Bcl-2 blocks apoptotic signal of transforming growth factor-beta in human hepatoma cells
    作者: Huang, YL;Chou, CK
    貢獻者: Division of Molecular and Genomic Medicine
    摘要: Transforming growth factor-beta (TGF-beta) has been shown to induce apoptosis on normal hepatocytes and hepatoma cells both in vitro and in vivo. However, how the TGF-beta induces apoptosis is still not clear. We examined the expression of anti-apoptosis proteins and sensitivity to TGF-beta in three well differentiated human hepatoma cell lines. Two TGF-beta sensitive cell lines Hep3B and HuH7 totally lacked Bcl-2. In contrast, the TGF-beta resistant HepG2 cells expressed a substantial amount of Bcl-2. AU three cell lines expressed equal amounts of Bcl-X-L, Bcl-X-S and Bar. Overexpression of Bcl-2 in Hep3B and HuH7 cells protected them from TGF-beta-induced apoptosis. TGF-beta treatment increased intracellular peroxide production and suppressed the expression of glutathione-S-transferase in the Hep3B cells, and these effects were partially suppressed by the overexpression of Bcl-2. These results suggest that Bcl-2 may protect cell from TGF-beta-F-induced apoptosis by interfering TGF-beta generated signals leading to induce reactive oxygen species production.
    關鍵詞: Medicine, Research & Experimental
    日期: 1998-05
    關聯: Journal of Biomedical Science. 1998 May;5(3):185-191.
    Link to: http://dx.doi.org/10.1007/BF02253468
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1021-7770&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000074668700004
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0031810265
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