The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis
Open accessAbstract
The p53 protein is mutated in about 50% of human cancers. Aside from losing the tumor-suppressive functions of the wild-type form, mutant p53 proteins often acquire inherent, novel oncogenic functions, a phenomenon termed mutant p53 gain-of-function (GOF). A growing body of evidence suggests that these pro-oncogenic functions of mutant p53 proteins are mediated by affecting the transcription of various genes, as well as by protein–protein interactions with transcription factors and other effectors. In the current review, we discuss the various GOF effects of mutant p53, and how it may serve as a central node in a network of genes and proteins, which, altogether, promote the tumorigenic process. Finally, we discuss mechanisms by which “Mother Nature” tries to abrogate the pro-oncogenic functions of mutant p53. Thus, we suggest that targeting mutant p53, via its reactivation to the wild-type form, may serve as a promising therapeutic strategy for many cancers that harbor mutant p53. Not only will this strategy abrogate mutant p53 GOF, but it will also restore WT p53 tumor-suppressive functions.
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Citations
Cites
Modulation of oxidative stress as an anticancer strategy
Gorrini, C., Harris, I. S., & Mak, T. W. (2013) · Nature Reviews Drug Discovery · doi:10.1038/nrd4002 · Cited by 3,579
TP53 mutations in human cancers: origins, consequences, and clinical use.
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“Most of these mutations are found in the DNA-binding domain (DBD) of p53 and abrogate its transcriptional activity [16].”
BackgroundThe first 30 years of p53: growing ever more complex.
Levine, A. J., & Oren, M. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2723 · Cited by 1,967
Mutant p53 in Cancer: New Functions and Therapeutic Opportunities
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Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
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Suppression of induced pluripotent stem cell generation by the p53–p21 pathway
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Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function
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When mutants gain new powers: News from the mutant p53 field
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Self-citationLinking the p53 tumour suppressor pathway to somatic cell reprogramming
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A p53-mediated DNA damage response limits reprogramming to ensure iPS cell genomic integrity
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Cited by
Drugs Targeting p53 Mutations with FDA Approval and in Clinical Trials
Nishikawa, S., & Iwakuma, T. (2023) · Cancers · doi:10.3390/cancers15020429 · Cited by 115
Vodicka, P., Andera, L., Opattova, A., & Vodickova, L. (2021) · Cancers · doi:10.3390/cancers13030479 · Cited by 39
McCubrey, J. A., Meher, A. K., Akula, S. M., Abrams, S. L., Steelman, L. S., LaHair, M. M., Franklin, R. A., Martelli, A. M., Ratti, S., Cocco, L., et al. (2022) · Aging · doi:10.18632/aging.204038 · Cited by 12
Metadata
- Authors
- Stein, Y., Rotter, V., & Aloni-Grinstein, R.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2019-12-08
- Volume
- 20
- Issue
- 24
- Pages
- 6197
- ISSN
- 1422-0067 (ISSN-L)
- OpenAlex
- W2993448515
- Cited by
- 162
- References
- 28
- FWCI
- 7.16
- Type
- journal article
- Language
- en
- Open access
- gold
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- Stein, Y., Rotter, V., & Aloni-Grinstein, R. (2019). Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms20246197
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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