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The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression
被引:831
作者:

Chen, Jiandong
论文数: 0 引用数: 0
h-index: 0
机构:
H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA
机构:
[1] H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL 33612 USA
基金:
美国国家卫生研究院;
关键词:
DNA-BINDING DOMAIN;
TERMINAL PROLIFERATION ARREST;
ACTIVITY IN-VIVO;
GENE-EXPRESSION;
P53-DEPENDENT APOPTOSIS;
POTENTIAL MEDIATOR;
THERAPEUTIC TARGET;
MDM2;
ANTAGONISTS;
CANCER-THERAPY;
SENESCENCE;
D O I:
10.1101/cshperspect.a026104
中图分类号:
R-3 [医学研究方法];
R3 [基础医学];
学科分类号:
1001 ;
摘要:
P53 is a transcription factor highly inducible by many stress signals such as DNA damage, oncogene activation, and nutrient deprivation. Cell-cycle arrest and apoptosis are the most prominent outcomes of p53 activation. Many studies showed that p53 cell-cycle and apoptosis functions are important for preventing tumor development. p53 also regulates many cellular processes including metabolism, antioxidant response, and DNA repair. Emerging evidence suggests that these noncanonical p53 activities may also have potent antitumor effects within certain context. This review focuses on the cell-cycle arrest and apoptosis functions of p53, their roles in tumor suppression, and the regulation of cell fate decision after p53 activation.
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