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The MDM2/MDMX/p53 axis in the adaptive stress response.

Bing Wang1,2,3, Cody Rasmussen-Ivey3, John B Little3

  • 1Key Laboratory of Space Radiobiology of Gansu Province & Key Laboratory of Heavy Ion Radiation Biology and Medicine of Chinese Academy of Sciences, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China.

Translational Cancer Research
|February 4, 2022
PubMed
Summary

The tumor suppressor p53 (also known as TP53) can promote cell survival during stress. However, chronic stress leads to p53 decline, potentially causing permanent loss of its function and homeostasis.

Keywords:
The MDM2/MDMX/p53 axisadaptive stress responsecell fatemild stress

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Area of Science:

  • Cellular biology
  • Molecular oncology
  • Stress response pathways

Background:

  • The p53 protein (also known as TP53) is a key regulator of cellular stress responses, traditionally recognized for its role in inducing cell death.
  • Emerging evidence suggests p53 also plays a crucial role in promoting cell survival through adaptive stress responses.

Purpose of the Study:

  • To elucidate the dual role of p53 in cellular stress, encompassing both pro-death and pro-survival functions.
  • To investigate the relationship between adaptive stress responses, p53 dynamics, and the maintenance of cellular homeostasis.

Main Methods:

  • Review and synthesis of existing literature on p53 function in cellular stress.
  • Analysis of the impact of stress intensity and duration on p53 activity and abundance.
  • Modeling of p53-mediated cell fate determination under varying stress conditions.

Main Results:

  • Adaptive stress responses are linked to a transient decline in p53 levels, which is necessary for activating pro-survival pathways.
  • Persistent or chronic adaptive stress responses can lead to sustained downregulation of p53.
  • This sustained p53 loss results in impaired homeostasis and a permanent deficit in p53-dependent functions.

Conclusions:

  • Cellular fate decisions under stress are governed by the interplay between stress levels, stress duration, and p53 regulation.
  • The dynamic regulation of p53 abundance and activity is critical for balancing cell survival and death.
  • Chronic stress-induced p53 downregulation poses a risk to cellular homeostasis and function.