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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

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Regulation of p53 stability as a therapeutic strategy for cancer

Zhifei Xu1, Wentong Wu1, Hao Yan1

  • 1Center for Drug Safety Evaluation and Research of Zhejiang University, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China.

Biochemical Pharmacology
|January 9, 2021
PubMed

Insights

This review explores how compounds degrade the tumor suppressor protein p53, crucial for cell death and homeostasis. Understanding p53 stability regulation offers new therapeutic strategies for cancer and other diseases.

Area of Science:

  • Molecular Biology
  • Biochemistry
  • Oncology

Background:

  • The tumor suppressor protein p53 regulates vital biological functions including cell death, metabolic homeostasis, and immune responses.
  • Mutations in the p53 gene occur in about 50% of human cancers, leading to oncogenic functions that promote tumor progression and chemoresistance.
  • Precise regulation of both wild-type and mutant p53 stability is essential for normal cellular functions and represents a key therapeutic target in cancer treatment.

Purpose of the Study:

  • To review compound-induced degradation of p53 through proteasome and autophagy-lysosome pathways.
  • To discuss other post-translational modifications influencing p53 stability and biological functions.
  • To provide a theoretical basis for p53 abundance regulation and its therapeutic applications in various diseases.

Main Methods:

  • Literature review focusing on compound-induced p53 degradation mechanisms.
  • Analysis of ubiquitination-dependent proteasome and autophagy-lysosome pathways in p53 regulation.
  • Examination of various post-translational modifications affecting p53 stability.

Main Results:

  • Compounds can induce p53 degradation via both the ubiquitination-dependent proteasome and autophagy-lysosome pathways.
  • Post-translational modifications significantly control p53 stability and its associated biological functions.
  • Targeting p53 stability through compound-induced degradation is a promising therapeutic strategy.

Conclusions:

  • The regulation of p53 stability is critical for maintaining normal cellular functions and preventing diseases like cancer.
  • Understanding the mechanisms of p53 degradation offers potential therapeutic avenues for cancer and other p53-related disorders.
  • This review consolidates current knowledge on p53 stability regulation, highlighting its implications for disease treatment.
Keywords:
AutophagyP53Posttranslational modificationProteasomeStabilityTherapeutic strategyUbiquitination

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