p53 and ARF: unexpected players in autophagy

被引:89
作者
Balaburski, Gregor M. [1 ]
Hontz, Robert D. [1 ]
Murphy, Maureen E. [1 ]
机构
[1] Fox Chase Canc Ctr, Program Mol & Translat Med, Philadelphia, PA 19111 USA
基金
美国国家卫生研究院;
关键词
TUMOR-SUPPRESSOR; DEPENDENT INDUCTION; MITOCHONDRIAL P-32; CELL-SURVIVAL; CANCER; INHIBITION; APOPTOSIS; P19(ARF); DEATH; SMARF;
D O I
10.1016/j.tcb.2010.02.007
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
p53 and ARF are well-established tumor-suppressor proteins that function together in the negative regulation of cancer. Recently, both proteins were found to play surprising roles in autophagy. Autophagy eating') is a crucial response of eukaryotic cells to metabolic and other stress. During this process, portions of the cytosol are sequestered into characteristic double-membrane vesicles that are delivered to the lysosome for degradation, leading to the release of free amino acids and promoting cell survival. The mechanisms whereby p53 and ARF control autophagy are only now becoming elucidated. An emerging question is whether we can develop metabolic poisons that preferentially destroy tumor cells depending on their reliance on autophagy for survival, and on their p53 and ARF status.
引用
收藏
页码:363 / 369
页数:7
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