The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression

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 fo...

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Bibliographic Details
Published inCold Spring Harbor perspectives in medicine Vol. 6; no. 3; p. a026104
Main Author Chen, Jiandong
Format Journal Article
LanguageEnglish
Published United States Cold Spring Harbor Laboratory Press 01.03.2016
Subjects
Animals
Apoptosis - physiology
Cell Cycle Checkpoints - physiology
DNA Repair
Mice
Neoplasms - prevention & control
Transcription Factors
Transcriptional Activation
Tumor Suppressor Protein p53 - metabolism
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Summary: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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ISSN:2157-1422
2472-5412
DOI:10.1101/cshperspect.a026104