p53 Retards cell-growth and suppresses etoposide-induced apoptosis in Pin1-deficient mouse embryonic fibroblasts.
p53 Retards cell-growth and suppresses etoposide-induced apoptosis in Pin1-deficient mouse embryonic fibroblasts.
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DOI：
10.1016/j.bbrc.2012.04.121
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发表时间：
2012-05
影响因子：
3.1
通讯作者：
K. Shimazaki;T. Uchida;A. Komine;Katsuhiko Takahashi
中科院分区：
文献类型：
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作者：
K. Shimazaki;T. Uchida;A. Komine;Katsuhiko Takahashi
我们通过用依托泊苷处理原代小鼠胚胎成纤维细胞 (MEF)，研究了 Pin1（肿瘤抑制剂 p53 的调节分子）对细胞周期停滞和细胞凋亡的影响。依托泊苷在野生型和 Pin1 缺失 (pin1−/−) MEF 中诱导 G1 期停滞，在仅缺乏 p53 (p53−/−) 或同时缺乏 Pin1 和 p53 (pin1−/−p53−/−) 的 MEF 中诱导 G2/M 期停滞和细胞凋亡。 pin1−/− 和 pin1−/−p53−/−MEF 都增强了线粒体中细胞色素 c 的释放，这可能会诱导细胞凋亡。作为依托泊苷治疗的反应，pin1−/−p53−/−MEF 中出现细胞凋亡，但 pin1−/−MEF 中未出现细胞凋亡。这些结果表明，p53 会延缓 pin1−/−MEF 的生长并抑制依托泊苷诱导的细胞凋亡。
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.