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Hyperphosphorylated PTEN exerts oncogenic properties.

Janine H van Ree1, Karthik B Jeganathan1, Raul O Fierro Velasco1

  • 1Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, MN, USA.

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|May 24, 2023
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Altered PTEN C-tail phosphorylation can create oncogenic PTEN, driving cancer growth. Targeting this C-tail hyperphosphorylation offers a potential anti-cancer therapy strategy.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • PTEN is a critical tumor suppressor sensitive to expression and functional changes.
  • The PTEN C-tail domain's role in tumorigenesis is unclear despite its involvement in PTEN stability, localization, activity, and interactions.

Purpose of the Study:

  • To investigate the role of PTEN C-tail phosphorylation in tumorigenesis.
  • To determine how specific phosphorylation events on the PTEN C-tail influence its tumor-suppressive functions.

Main Methods:

  • Utilized mouse models with specific C-tail mutations (deletions, nonphosphorylatable, and phosphomimetic variants).
  • Analyzed PTEN levels, AKT activity, and tumorigenic potential in these mouse strains.
  • Examined the impact of S380 phosphorylation dynamics on PTEN stability and PI3K-AKT inhibition.

Main Results:

  • Deletion of C-tail sites (S370, S380, T382, T383) led to low PTEN and hyperactive AKT but did not promote tumors.
  • Phosphorylation dynamics at S380 are crucial for PTEN stability and PI3K-AKT pathway inhibition.
  • A phosphomimetic S380 variant promoted prostate cancer growth via nuclear beta-catenin accumulation, while a nonphosphorylatable S380 variant was not tumorigenic.

Conclusions:

  • PTEN C-tail hyperphosphorylation can paradoxically create an oncogenic form of PTEN.
  • Dynamic phosphorylation of the PTEN C-tail, particularly at S380, is essential for its tumor suppressor activity.
  • PTEN C-tail hyperphosphorylation represents a potential therapeutic target for cancer treatment.