MEDIATION OF C-MYC-INDUCED APOPTOSIS BY P53
MEDIATION OF C-MYC-INDUCED APOPTOSIS BY P53
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DOI：
10.1126/science.8091232
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发表时间：
1994-09-30
期刊：
影响因子：
56.9
通讯作者：
EICK, D
中科院分区：
文献类型：
--
作者：
HERMEKING, H;EICK, D
细胞原癌基因c-myc参与细胞增殖和转化，但也参与诱导程序性细胞死亡（凋亡）。肿瘤抑制基因p53（人类癌症中最常见的突变基因）也具有相同的特征。在表达野生型p53蛋白的静止小鼠成纤维细胞中，发现c-Myc的激活诱导细胞凋亡和细胞周期重新进入，之前是p53的稳定。相反，在静止的p53无效的成纤维细胞中，c-Myc的激活诱导细胞周期重新进入，但不诱导细胞凋亡。这些结果表明，p53介导的细胞凋亡作为一种保护机制，以防止癌基因激活诱导的细胞增殖。
The cellular proto-oncogene c-myc is involved in cell proliferation and transformation but is also implicated in the induction of programmed cell death (apoptosis). The same characteristics have been described for the tumor suppressor gene p53, the most commonly mutated gene in human cancer. In quiescent mouse fibroblasts expressing wildtype p53 protein, activation of c-Myc was found to induce apoptosis and cell cycle reentry, preceded by stabilization of p53. In contrast, in quiescent p53-null fibroblasts, activation of c-Myc induced cell cycle reentry but not apoptosis. These results suggest that p53 mediates apoptosis as a safeguard mechanism to prevent cell proliferation induced by oncogene activation.