E2F1 and c-Myc in Cell Growth and Death

被引:147
作者
Matsumura, Itaru [1 ]
Tanaka, Hirokazu [1 ]
Kanakura, Yuzuru [1 ]
机构
[1] Osaka Univ, Grad Sch Med, Dept Hematol Oncol, 2-2 Yamada Oka, Suita, Osaka 5650871, Japan
关键词
E2F1; c-Myc; apoptosis; NF-_B; p53; ROS;
D O I
10.4161/cc.2.4.428
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cell cycle machinery controls not only cell growth but also cell survival and death. For example, overexpression of c-Myc or E2F1, which are involved in G(1)/S transition, causes apoptosis under certain conditions. Furthermore, endogenous E2F1 also participates in apoptosis, as evidenced by the defect of apoptosis in E2F1-deficient mice. Candidate molecules that mediate c-Myc-and E2F1-enhanced apoptosis include p14/p19(ARF), ornithine decarboxylase and lactate degydrogenase-A (for c-Myc) as well as p14/p19(ARF), p73, Apaf-1 and caspase-3 (for E2F1). c-Myc also activates the CD95/Fas-FADD-mediated death signal. c-Myc and E2F1 inhibit NF-kappa B activities induced by TNF alpha or reactive oxygen species. Therefore, c-Myc and E2F1 regulate cell growth and death not only by inducing transcription but also by modulating signal transduction pathways.
引用
收藏
页码:333 / 338
页数:6
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