کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2115784 1084610 2006 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hepatitis B virus X protein induces apoptosis in hepatoma cells through inhibiting Bcl-xL expression
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی تحقیقات سرطان
پیش نمایش صفحه اول مقاله
Hepatitis B virus X protein induces apoptosis in hepatoma cells through inhibiting Bcl-xL expression
چکیده انگلیسی

The X protein of hepatitis B virus (HBx) exhibits numerous activities affecting gene transcription, intracellular signal transduction, cell proliferation and apoptosis. Recent studies showed that HBx induced apoptosis by causing loss of mitochondrial membrane potential, suggesting that HBx-mediated apoptosis is mitochondria-dependent. However, the molecular mechanism of the gene in this pathway is still far from understood. In this study, we demonstrated that introduction of HBx into a hepatocellular carcinoma cell line, Hep3B, caused apoptosis and sensitized the cell to TNFα-induced cell killing. Over-expression of Bcl-xL, an anti-apoptotic Bcl-2 family protein, prevented cell death dragged by HBx. Importantly, expression of HBx in Hep3B cells reduced Bcl-xL mRNA and protein levels, but did not regulate other Bcl-2 family members. Although, HBx itself did not affect intracellular distribution of cytochrome c, an enhanced release of cytochrome c from mitochondria was observed when TNFα was applied. Thus, the introduction of HBx into Hep3B cells induces apoptosis and sensitizes Hep3B cells to TNFα-mediated cell killing, and these processes may accomplish through inhibiting Bcl-xL expression and subsequently promoting cytochrome c release from mitochondria.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cancer Letters - Volume 236, Issue 1, 8 May 2006, Pages 115–124
نویسندگان
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