p53 Retards cell-growth and suppresses etoposide-induced apoptosis in Pin1-deficient mouse embryonic fibroblasts

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• 作者：Kiyoe Shimazaki^a ; Takafumi Uchida^b ; ^c ; ^{uchidat@biochem.tohoku.ac.jp} ; Akihiko Komine^b ; Katsuhiko Takahashi^a ; ^c ; ^d
• 关键词：Apoptosis ; Etoposide ; Mitochondria ; p53 ; Pin1
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：25 May, 2012
• 卷：422
• 期：1
• 页码：133-138
• 文件大小：582 K

摘要

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^{鈭?鈭?/sup>) MEFs, and G2/M arrest and apoptotic cell death in MEFs lacking either p53 only (p53鈭?鈭?/sup>) or both Pin1 and p53 (pin1鈭?鈭?/sup>p53鈭?鈭?/sup>). Both pin1鈭?鈭?/sup> and pin1鈭?鈭?/sup>p53鈭?鈭?/sup> 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鈭?鈭?/sup>p53鈭?鈭?/sup> MEFs but not in pin1鈭?鈭?/sup> MEFs. These results suggest that p53 retards growth and suppresses etoposide-induced apoptosis in pin1鈭?鈭?/sup> MEFs.}