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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
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The PTEN/NRF2 axis promotes human carcinogenesis.

Ana I Rojo1, Patricia Rada, Marta Mendiola

  • 11 Department of Biochemistry, Faculty of Medicine, Autonomous University of Madrid , and Instituto de Investigaciones Biomédicas "Alberto Sols" UAM-CSIC, Madrid, Spain .

Antioxidants & Redox Signaling
|June 4, 2014
PubMed
Summary
This summary is machine-generated.

Loss of the tumor suppressor PTEN increases activity of the transcription factor NRF2, promoting cancer growth. This PTEN/NRF2 pathway is crucial in human carcinogenesis and offers a new therapeutic target.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The tumor suppressor PTEN normally inhibits cellular growth and proliferation.
  • Previous studies in mice showed PTEN loss enhances NRF2 activity in the liver.
  • The precise mechanism and relevance of PTEN's control over NRF2 in human cancer remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanism by which PTEN regulates NRF2.
  • To investigate the role of the PTEN-NRF2 pathway in human carcinogenesis, particularly in endometrioid carcinomas.

Main Methods:

  • Utilized drug and genetic targeting of PTEN.
  • Employed phosphoproteomics to identify NRF2 phosphorylation sites.
  • Conducted rescue experiments in PTEN-deficient cells.
  • Analyzed tissue microarrays from human endometrioid carcinomas.

Main Results:

  • PTEN loss leads to GSK-3-mediated phosphorylation of NRF2 at Ser335/338, promoting its degradation via β-TrCP.
  • Loss of PTEN results in increased NRF2 activity, conferring a proliferative and tumorigenic advantage.
  • PTEN-negative endometrioid carcinomas frequently exhibit high NRF2 or HO-1 expression (80% of cases).

Conclusions:

  • Uncovered a novel mechanism where PTEN loss activates NRF2 oncogenic potential through GSK-3/β-TrCP.
  • The PTEN/NRF2 pathway is a significant driver in human carcinogenesis, including endometrioid carcinomas.
  • Targeting the NRF2 pathway represents a promising therapeutic strategy for PTEN-deficient cancers.