The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Mutant p53 as a guardian of the cancer cell
Open accessAbstract
Forty years of research have established that the p53 tumor suppressor provides a major barrier to neoplastic transformation and tumor progression by its unique ability to act as an extremely sensitive collector of stress inputs, and to coordinate a complex framework of diverse effector pathways and processes that protect cellular homeostasis and genome stability. Missense mutations in the TP53 gene are extremely widespread in human cancers and give rise to mutant p53 proteins that lose tumor suppressive activities, and some of which exert trans-dominant repression over the wild-type counterpart. Cancer cells acquire selective advantages by retaining mutant forms of the protein, which radically subvert the nature of the p53 pathway by promoting invasion, metastasis and chemoresistance. In this review, we consider available evidence suggesting that mutant p53 proteins can favor cancer cell survival and tumor progression by acting as homeostatic factors that sense and protect cancer cells from transformation-related stress stimuli, including DNA lesions, oxidative and proteotoxic stress, metabolic inbalance, interaction with the tumor microenvironment, and the immune system. These activities of mutant p53 may explain cancer cell addiction to this particular oncogene, and their study may disclose tumor vulnerabilities and synthetic lethalities that could be exploited for hitting tumors bearing missense TP53 mutations.
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“Mutant p53 may not only lose the tumor suppressor function of wild-type p53 but also acquire new tumor-promoting functions, such as promoting tumor invasion, metastasis, and drug resistance.”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [494]
In the citing paper
“mutant p53 GOF activities, including the facilitation of cell proliferation, invasion, survival, cancer-promoting metabolism, protumorigenic inflammation, and drug resistance, have been observed in a series of experimental models, and multiple GOF mechanisms have been proposed.140,493,494”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [494]
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Cites
The emerging hallmarks of cancer metabolism
Pavlova, N. N., & Thompson, C. B. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.12.006 · Cited by 5,926 · cited 1×
“tumor growth in hypoxic conditions and contributes to suppress immune surveillance through extracellular acidification [33].”
P53 in survival, death and metabolic health: a lifeguard with a licence to kill.
Kruiswijk, F., Labuschagne, C. F., & Vousden, K. H. (2015) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm4007 · Cited by 1,080
Targeting mutant p53 for efficient cancer therapy
Bykov, V. J. N., Eriksson, S. E., Bianchi, J., & Wiman, K. G. (2018) · Nature Reviews Cancer · doi:10.1038/nrc.2017.109 · Cited by 889
Tumour-associated mutant p53 drives the Warburg effect
Zhang, C., Liu, J., Liang, Y., Wu, R., Zhao, Y., Hong, X., Lin, M., Yu, H., Liu, L., Levine, A. J., et al. (2013) · Nature Communications · doi:10.1038/ncomms3935 · Cited by 434
Walerych, D., Lisek, K., Sommaggio, R., Piazza, S., Ciani, Y., Dalla, E., Rajkowska, K., Gaweda-Walerych, K., Ingallina, E., Tonelli, C., et al. (2016) · Nature Cell Biology · doi:10.1038/ncb3380 · Cited by 239
Peng, X., Zhang, M.-Q.-Z., Conserva, F., Hosny, G., Selivanova, G., Bykov, V. J. N., Arnér, E. S. J., & Wiman, K. G. (2013) · Cell Death & Disease · doi:10.1038/cddis.2013.417 · Cited by 170
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Mutant p53 promotes tumor progression and metastasis by the endoplasmic reticulum UDPase ENTPD5
Vogiatzi, F., Brandt, D. T., Schneikert, J., Fuchs, J., Grikscheit, K., Wanzel, M., Pavlakis, E., Charles, J. P., Timofeev, O., Nist, A., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1612711114 · Cited by 99
Cited by
Targeting p53 pathways: mechanisms, structures, and advances in therapy
Wang, H., Guo, M., Wei, H., & Chen, Y. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01347-1 · Cited by 1,016
Yun, J., Lee, S.-H., Kim, S.-Y., Jeong, S.-Y., Kim, J.-H., Pyo, K.-H., Park, C.-W., Heo, S. G., Yun, M. R., Lim, S., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-20-0116 · Cited by 297
Hu, H.-F., Ye, Z., Qin, Y., Xu, X.-W., Yu, X.-J., Zhuo, Q.-F., & Ji, S.-R. (2021) · Acta Pharmacologica Sinica · doi:10.1038/s41401-020-00584-2 · Cited by 149
Regulation of Adult Neurogenesis in Mammalian Brain
Niklison-Chirou, M. V., Agostini, M., Amelio, I., & Melino, G. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21144869 · Cited by 143
Haupt, S., Caramia, F., Herschtal, A., Soussi, T., Lozano, G., Chen, H., Liang, H., Speed, T. P., & Haupt, Y. (2019) · Nature Communications · doi:10.1038/s41467-019-13266-3 · Cited by 94
Metadata
- Authors
- Mantovani, F., Collavin, L., & Del Sal, G.
- Venue
- Cell Death & Differentiation
- Published
- 2018-12-11
- Volume
- 26
- Issue
- 2
- Pages
- 199-212
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W2904049988
- Cited by
- 775
- References
- 8
- FWCI
- 22.83
- Type
- journal article
- Language
- en
- Open access
- hybrid
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