The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Gain-of-function mutant p53 in cancer progression and therapy
Open accessAbstract
p53 is a key tumor suppressor, and loss of p53 function is frequently a prerequisite for cancer development. The p53 gene is the most frequently mutated gene in human cancers; p53 mutations occur in >50% of all human cancers and in almost every type of human cancers. Most of p53 mutations in cancers are missense mutations, which produce the full-length mutant p53 (mutp53) protein with only one amino acid difference from wild-type p53 protein. In addition to loss of the tumor-suppressive function of wild-type p53, many mutp53 proteins acquire new oncogenic activities independently of wild-type p53 to promote cancer progression, termed gain-of-function (GOF). Mutp53 protein often accumulates to very high levels in cancer cells, which is critical for its GOF. Given the high mutation frequency of the p53 gene and the GOF activities of mutp53 in cancer, therapies targeting mutp53 have attracted great interest. Further understanding the mechanisms underlying mutp53 protein accumulation and GOF will help develop effective therapies treating human cancers containing mutp53. In this review, we summarize the recent advances in the studies on mutp53 regulation and GOF as well as therapies targeting mutp53 in human cancers.
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Cites
p53 Regulates Mitochondrial Respiration
Matoba, S., Kang, J.-G., Patino, W. D., Wragg, A., Boehm, M., Gavrilova, O., Hurley, P. J., Bunz, F., & Hwang, P. M. (2006) · Science · doi:10.1126/science.1126863 · Cited by 1,650
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Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
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BackgroundPRIMA-1 reactivates mutant p53 by covalent binding to the core domain
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Human pluripotent stem cells recurrently acquire and expand dominant negative P53 mutations
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Mutant p53 Drives Pancreatic Cancer Metastasis through Cell-Autonomous PDGF Receptor β Signaling
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BackgroundA dominant-negative effect drives selection of TP53 missense mutations in myeloid malignancies
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Cited by
Mutant p53 in cancer: from molecular mechanism to therapeutic modulation
Chen, X., Zhang, T., Su, W., Dou, Z., Zhao, D., Jin, X., Lei, H., Wang, J., Xie, X., Cheng, B., et al. (2022) · Cell Death & Disease · doi:10.1038/s41419-022-05408-1 · Cited by 494
Self-citationMutations of p53 associated with pancreatic cancer and therapeutic implications
Voutsadakis, I. A. (2021) · Annals of Hepato-Biliary-Pancreatic Surgery · doi:10.14701/ahbps.2021.25.3.315 · Cited by 75
McCubrey, J. A., Yang, L. V., Abrams, S. L., Steelman, L. S., Follo, M. Y., Cocco, L., Ratti, S., Martelli, A. M., Augello, G., & Cervello, M. (2022) · Cells · doi:10.3390/cells11142155 · Cited by 49
Vodicka, P., Andera, L., Opattova, A., & Vodickova, L. (2021) · Cancers · doi:10.3390/cancers13030479 · Cited by 39
Zhong, G., Zhao, Y., Zhuang, D., Chung, W. K., & Shen, Y. (2025) · Nature Communications · doi:10.1038/s41467-025-62318-4 · Cited by 15
Metadata
- Authors
- Zhang, C., Liu, J., Xu, D., Zhang, T., Hu, W., & Feng, Z.
- Venue
- Journal of Molecular Cell Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2020-07-28
- Volume
- 12
- Issue
- 9
- Pages
- 674-687
- ISSN
- 1674-2788 (ISSN-L)
- 1759-4685
- OpenAlex
- W3045935025
- Cited by
- 334
- References
- 24
- FWCI
- 11.71
- Type
- journal article
- Language
- en
- Open access
- gold
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
