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A balancing act: PHLPP2 fine tunes AKT activity and MYC stability in prostate cancer

Roxanne Toivanen1,2,3, Luc Furic4,2,3

  • 1Cancer Program, Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Clayton, Victoria, Australia roxanne.toivanen@petermac.org.

The Journal of Cell Biology
|May 31, 2019
PubMed

Insights

Loss of PTEN and p53 in prostate cancer surprisingly activates MYC stability. The phosphatase PHLPP2, which normally suppresses AKT, unexpectedly drives disease progression in this context.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Prostate tumor progression is often driven by Phosphatase and tensin homolog (PTEN) loss, which sustains AKT activation.
  • Tumor suppressor p53 loss is also common in advanced cancers, including prostate cancer.

Purpose of the Study:

  • To investigate the role of the AKT-suppressing phosphatase PHLPP2 in prostate cancer progression under conditions of dual PTEN and p53 loss.
  • To elucidate the molecular mechanisms by which PHLPP2 influences tumor growth in this specific genetic context.

Main Methods:

  • Utilized mouse models of prostate cancer with combined PTEN and p53 deficiency.
  • Assessed the impact of PHLPP2 levels on tumor growth, AKT signaling, and MYC protein stability.
  • Employed molecular biology techniques to analyze protein interactions and degradation pathways.

Main Results:

  • Contrary to expectations, PHLPP2 was found to promote prostate tumor progression when both PTEN and p53 were lost.
  • PHLPP2 increased the stability of MYC oncoprotein, leading to enhanced tumor growth.
  • The phosphatase's activity in this context was independent of its canonical AKT-suppressing function.

Conclusions:

  • PHLPP2 plays a pro-tumorigenic role in PTEN/p53-deficient prostate cancer by stabilizing MYC.
  • These findings reveal a novel mechanism linking PHLPP2, MYC stability, and prostate cancer pathogenesis.
  • Targeting PHLPP2 or MYC could offer new therapeutic strategies for advanced prostate cancer with dual PTEN and p53 loss.

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