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Gata3 antagonizes cancer progression in Pten-deficient prostates

Alana H T Nguyen1, Mathieu Tremblay, Katharina Haigh

  • 1Goodman Cancer Research Centre and Department of Biochemistry, McGill University, Montreal, Quebec, Canada H3A 1A3.

Human Molecular Genetics
|February 23, 2013
PubMed

Insights

Loss of Gata3 transcription factor accelerates prostate cancer invasion in Pten-deficient mice. Restoring GATA3 delays tumor progression and prevents Akt activation, suggesting GATA3 is a key regulator.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Loss of the tumor suppressor PTEN is frequent in prostate cancer, activating the PI3K-Akt pathway and promoting tumor growth.
  • The transcription factor Gata3 is progressively lost in Pten-deficient prostate tumors through reduced transcription and increased degradation.

Purpose of the Study:

  • To investigate the role of Gata3 in prostate cancer progression in Pten-deficient models.
  • To determine the clinical significance of GATA3 expression in human prostate tumors.

Main Methods:

  • Utilized conditional loss- and gain-of-function approaches to manipulate Gata3 expression in mouse prostate tumors.
  • Analyzed Gata3 expression and Akt activation in Pten-deficient prostates.
  • Correlated GATA3 levels with tumor stage and recurrence in human prostate cancer samples.

Main Results:

  • Gata3 inactivation accelerated tumor invasion in Pten-deficient prostates.
  • Enforced GATA3 expression delayed tumor progression and prevented Akt activation.
  • Down-regulation of Pik3cg and Pik3c2a mRNAs was observed with enforced GATA3.
  • Human prostate tumors show loss of active GATA3 during progression to castrate-resistant stages.
  • GATA3 levels predict recurrence in hormone-sensitive tumors.

Conclusions:

  • Gata3 acts as a crucial regulator of prostate cancer progression.
  • Loss of GATA3 contributes to prostate cancer advancement by promoting PI3K-Akt pathway activation.
  • GATA3 status is a potential biomarker for prostate cancer recurrence and progression.

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