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Updated: Apr 6, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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PP2A inhibition as a novel therapeutic target in castration-resistant prostate cancer

Paula González-Alonso1, Ion Cristóbal, Rebeca Manso

  • 1Pathology Department, IIS "Fundación Jiménez Diaz", Avda. Reyes Católicos-2, 28040, Madrid, Spain.

Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine
|August 4, 2015
PubMed

Insights

Protein phosphatase 2A (PP2A), a tumor suppressor, is often inhibited in prostate cancer. Its inactivation is linked to castration resistance, making PP2A a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Protein phosphatase 2A (PP2A) functions as a crucial tumor suppressor in various human cancers.
  • PP2A inactivation in prostate cancer is associated with alterations in its subunits and deregulation of inhibitors like CIP2A and SET.
  • Functional inactivation of PP2A is implicated in the development of castration-resistant prostate cancer.

Purpose of the Study:

  • To investigate the role of PP2A inactivation in prostate cancer progression.
  • To explore PP2A as a potential molecular target for treating castration-resistant prostate cancer.

Main Methods:

  • Analysis of PP2A subunit alterations.
  • Assessment of endogenous PP2A inhibitor levels (CIP2A, SET).
  • Correlation of PP2A functional status with castration-resistant phenotype.

Main Results:

  • PP2A subunits and inhibitors (CIP2A, SET) are frequently altered in prostate cancer.
  • PP2A inactivation is linked to the acquisition of castration resistance.
  • PP2A functional status is a key event in prostate cancer progression.

Conclusions:

  • PP2A inactivation is a significant mechanism contributing to prostate cancer development and progression.
  • Targeting PP2A offers a promising therapeutic strategy for castration-resistant prostate cancer.

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