The Cell–Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression
Open accessAbstract
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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Transcription factor p53 is the master regulator of the DNA damage response and is stabilized and transactivated in response to DNA damage.
“It is established that transcription factor p53 is the master regulator of the DNA damage response and is stabilized and transactivated in response to DNA damage [ 38 , 39 , 40 , 41 ].”
From Differential Induction of Reactive Oxygen Species and Expression of Antioxidant Enzymes in Human Melanocytes Correlate with Melanin Content: Implications on the Response to Solar UV and Melanoma Susceptibility (2022) · cites this paper as [39]
The Abstract (page unavailable) identifies p53 as a transcription factor induced by DNA damage. The Cell-Cycle Checkpoint Functions section (page unavailable) describes rapid p53 accumulation and induction of p21 after DNA double-strand breaks, supporting stabilization and transcriptional activation in that setting. It describes important checkpoint and repair functions, but does not establish the broader characterization of p53 as the master regulator of the DNA damage response. (LLM, conf=0.82)
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- Authors
- Chen, J.
- Affiliations
- Moffitt Cancer Center (US)
- Corresponding author
- Chen, Jiandong
- ORCID
- Chen, Jiandong
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2016-03
- Volume
- 6
- Issue
- 3
- Pages
- a026104
- ISSN
- 2157-1422 (ISSN-L)
- PMC
- PMC4772082
- OpenAlex
- W2288903023
- Cited by
- 1,222
- References
- 133
- Citations by year
- 2026: 75 · 2025: 164 · 2024: 161 · 2023: 175 · 2022: 199 · 2021: 180 · 2020: 143 · 2019: 72 · 2018: 22 · 2017: 21 · 2016: 9 · 2013: 1
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Florida Department of Health
- Moffitt Cancer Center (P30CA076292, CA076292)
- National Institutes of Health
- National Cancer Institute (R01CA109636, CA 109636, CA076292, CA141244, R01CA141244, P30CA076292)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- p53, cell cycle arrest, apoptosis, tumor initiation, tumor progression, tumor suppression, DNA damage response, oncogene activation, nutrient deprivation, cell fate determination, DNA repair, antioxidant response, metabolism
- MeSH terms
- Animals, DNA Repair, Neoplasms, Transcription Factors, Transcriptional Activation, Tumor Suppressor Protein p53, Apoptosis, Mice, Cell Cycle Checkpoints
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