کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1934087 1050633 2008 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Nuclear-factor-κB (NF-κB) and radical oxygen species play contrary roles in transforming growth factor-β1 (TGF-β1)-induced apoptosis in hepatocellular carcinoma (HCC) cells
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Nuclear-factor-κB (NF-κB) and radical oxygen species play contrary roles in transforming growth factor-β1 (TGF-β1)-induced apoptosis in hepatocellular carcinoma (HCC) cells
چکیده انگلیسی

Nuclear-Factor-κB (NF-κΒ can counteract transforming growth factor-β1 (TGF-β1)-induced apoptosis in malignant hepatocytes through up-regulation of its downstream genes, such as X-linked inhibitor of apoptosis protein (XIAP). Reports have demonstrated that TGF-β1 can induce oxidative stress, and c-Jun N-terminal Kinase1 (JNK1) is indispensable for TGF-β1-induced apoptosis pathway, but the relationship between radical oxygen species (ROS) and the activation of JNKs is still unclear. In the present study, we found that ROS can induce JNK activation in TGF-β1 mediated apoptosis in hepatocytes. The inhibitors of hydrogen peroxide and superoxide, which were produced by mitochondria under stress, could inhibit the phosphorylation of c-Jun in XIAP knockdown cells. In conclusion, it is the first time to show that both NF-κB and antioxidants can counteract TGF-β1-induced apoptosis in hepatic cell death through JNK1 pathway.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 377, Issue 4, 26 December 2008, Pages 1107–1112
نویسندگان
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