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Regulation of p53 stability as a therapeutic strategy for cancer.

Regulation of p53 stability as a therapeutic strategy for cancer.

Authors :
Xu, Zhifei
Wu, Wentong
Yan, Hao
Hu, Yuhuai
He, Qiaojun
Luo, Peihua
Source :
Biochemical Pharmacology. Mar2021, Vol. 185, pN.PAG-N.PAG. 1p.
Publication Year :
2021

Abstract

[Display omitted] The tumor suppressor protein p53 participates in the control of key biological functions such as cell death, metabolic homeostasis and immune function, which are closely related to various diseases such as tumors, metabolic disorders, infection and neurodegeneration. The p53 gene is also mutated in approximately 50% of human cancer cells. Mutant p53 proteins escape from the ubiquitination-dependent degradation, gain oncogenic function and promote the carcinogenesis, malignant progression, metastasis and chemoresistance. Therefore, the stability of both wild type and mutant p53 needs to be precisely regulated to maintain normal functions and targeting the p53 stability is one of the therapeutic strategies against cancer. Here, we focus on compound-induced degradation of p53 by both the ubiquitination-dependent proteasome and autophagy-lysosome degradation pathways. We also review other posttranslational modifications which control the stability of p53 and the biological functions involved in these processes. This review provides the current theoretical basis for the regulation of p53 abundance and its possible applications in different diseases. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00062952
Volume :
185
Database :
Academic Search Index
Journal :
Biochemical Pharmacology
Publication Type :
Academic Journal
Accession number :
149416572
Full Text :
https://doi.org/10.1016/j.bcp.2021.114407