کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1929732 | 1050472 | 2012 | 6 صفحه PDF | دانلود رایگان |
We studied the effects of Pin1, a regulatory molecule of the oncosuppressor p53, on both cell cycle arrest and apoptosis by treating primary mouse embryonic fibroblasts (MEFs) with etoposide. Etoposide induced G1 arrest in both wild-type and Pin1 null (pin1−/−) MEFs, and G2/M arrest and apoptotic cell death in MEFs lacking either p53 only (p53−/−) or both Pin1 and p53 (pin1−/−p53−/−). Both pin1−/− and pin1−/−p53−/− MEFs were enhanced the release of cytochrome c from the mitochondria, which might induce apoptosis. In response to etoposide treatment, apoptotic cell death was displayed in pin1−/−p53−/− MEFs but not in pin1−/− MEFs. These results suggest that p53 retards growth and suppresses etoposide-induced apoptosis in pin1−/− MEFs.
► Effect of Pin1 on apoptosis was studied by using pin1−/−p53−/− mouse cell.
► Pin1 inactivation facilitated apoptotic cell death in response to etoposide.
► An etoposide-induced apoptotic pathway was suppressed by p53 expression.
► Pin1 and/or p53 controls apoptosis at the post-mitochondrial level.
Journal: Biochemical and Biophysical Research Communications - Volume 422, Issue 1, 25 May 2012, Pages 133–138