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The Role of Tumor Suppressor p53 in the Antioxidant Defense and Metabolism
Open accessAbstract
Tumor suppressor p53 is inactivated in most cancers and the critical role of p53 in the suppression of carcinogenesis has been confirmed in many mouse models. The protein product of the tumor suppressor p53 gene works as a transcriptional regulator, activating expression of numerous genes involved in cell death, cell cycle arrest, senescence, DNA-repair and many other processes. In spite of the multiple efforts to characterize the functions of p53, the mechanisms of tumor suppression by p53 are still elusive. Recently, new activities of p53 such as regulation of reactive oxygen species (ROS) and metabolism have been described and the p53-regulated genes responsible for these functions have been identified. Metabolic derangements and accumulation of ROS are features of carcinogenesis, supporting the idea that many tumor suppressive effects of p53 can be mediated by regulation of metabolism and/or ROS. Mutations in the p53 gene can not only inactivate wild type function of p53 but also endow p53 with new functions such as activation of new metabolic pathways contributing to carcinogenesis. Understanding the metabolic and antioxidant functions of p53 allows us to develop approaches to restore p53 function in cancers, where p53 is inactivated, in other to ensure the best outcome of anti-cancer treatment.
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“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 ].”
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Self-citation
Metadata
- Authors
- Budanov, A. V.
- Affiliations
- Virginia Commonwealth University (US)
- Corresponding author
- Budanov, Andrei V.
- ORCID
- Budanov, Andrei V.
- Venue
- Subcellular Biochemistry
- Publisher
- Springer Netherlands
- Published
- 2014
- Volume
- 85
- Pages
- 337-358
- ISSN
- 0306-0225 (ISSN-L)
- PMC
- PMC4206257
- OpenAlex
- W13599526
- Cited by
- 157
- References
- 110
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 18 · 2023: 11 · 2022: 15 · 2021: 16 · 2020: 15 · 2019: 15 · 2018: 20 · 2017: 12 · 2016: 15 · 2015: 3 · 2014: 2
- FWCI
- 23.62
- Type
- book chapter
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Sub-cellular biochemistry/Subcellular biochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA172660)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- p53, tumor suppression, reactive oxygen species, antioxidant defense, cellular metabolism, carcinogenesis, p53 target genes, metabolic reprogramming, TP53 mutation, cancer therapy
- MeSH terms
- Antioxidants, DNA Repair, Humans, Mutation, Genes, p53, Reactive Oxygen Species, Oxidative Stress
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