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The Diverse Functions of Mutant 53, Its Family Members and Isoforms in Cancer
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Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis

Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 7610001, Israel
Department of Biochemistry and Molecular Genetics, Israel Institute for Biological Research, Ness-Ziona 7410001, Israel
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(24), 6197;
Received: 30 October 2019 / Revised: 25 November 2019 / Accepted: 5 December 2019 / Published: 8 December 2019
(This article belongs to the Special Issue p53 in Cancer and beyond—40 Years after Its Discovery)
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. View Full-Text
Keywords: mutant p53; gain of function; tumorigenesis; p53 reactivation; p53 network mutant p53; gain of function; tumorigenesis; p53 reactivation; p53 network
MDPI and ACS Style

Stein, Y.; Rotter, V.; Aloni-Grinstein, R. Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis. Int. J. Mol. Sci. 2019, 20, 6197.

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