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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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PI3K/Akt-mediated regulation of p53 in cancer

Aswin G Abraham1, Eric O'Neill1

  • 1*Cancer Research UK/MRC Oxford Institute, Gray Laboratories, Department of Oncology, University of Oxford, Old Road Campus, Roosevelt Drive, Oxford OX3 7DQ, U.K.

Biochemical Society Transactions
|August 12, 2014
PubMed

Insights

Cancer cells hijack the PI3K/Akt pathway to promote growth and survival. This pathway also impacts the TP53 tumor suppressor, influencing cancer treatment efficacy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is frequently activated in cancer, promoting cell proliferation and survival.
  • The TP53 tumor-suppressor gene is often inactivated in cancer, contributing to uncontrolled cell growth.
  • Akt typically inhibits p53 through MDM2-mediated degradation, a known mechanism in cancer.

Purpose of the Study:

  • To explore the complex regulatory mechanisms of p53 by the PTEN/PI3K/Akt pathway in cancer.
  • To discuss the implications of these regulatory mechanisms for the efficacy of clinical PI3K/Akt inhibitors.

Main Methods:

  • Literature review and synthesis of existing research on PI3K/Akt signaling and p53 regulation.
  • Analysis of emerging evidence on PTEN/PI3K/Akt-mediated p53 translation and protein stability.

Main Results:

  • While Akt often degrades p53 via MDM2, emerging evidence suggests PTEN/PI3K/Akt can also stabilize p53 under certain conditions.
  • These dual roles indicate complex Akt-mediated regulation of p53 in tumors.

Conclusions:

  • Understanding the multifaceted regulation of p53 by the PI3K/Akt pathway is critical for cancer therapy.
  • Assessing the impact of PI3K/Akt inhibitors on p53 activity is essential for predicting and improving therapeutic outcomes.

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