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Activation of PPARgamma increases PTEN expression in pancreatic cancer cells

Buckminster Farrow1, B Mark Evers

  • 1Department of Surgery, The University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555, USA.

Biochemical and Biophysical Research Communications
|January 22, 2003
PubMed

Insights

Activating PPARgamma increases the tumor suppressor PTEN, inhibiting PI3K activity in pancreatic cancer cells. This suggests a new therapeutic strategy for pancreatic cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The PI3K pathway is crucial for pancreatic cancer invasion and survival.
  • Peroxisome proliferator-activated receptor gamma (PPARgamma) has anti-tumor effects, but its tumor suppressive mechanisms are unclear.

Purpose of the Study:

  • To investigate if PPARgamma activation upregulates the tumor suppressor PTEN and inhibits PI3K signaling in pancreatic cancer.

Main Methods:

  • Utilized AsPC-1 human pancreatic cancer cells transfected with a PPRE-luciferase reporter construct.
  • Treated cells with PPARgamma ligands (e.g., rosiglitazone) and an inhibitor (GW9662).
  • Assessed PTEN expression and PI3K activity via phosphorylated Akt levels.

Main Results:

  • PPARgamma ligands activated the PPRE-luciferase construct, confirming functional PPARgamma.
  • Rosiglitazone significantly increased PTEN protein levels in AsPC-1 cells.
  • Inhibition of PPARgamma blocked the PTEN upregulation.
  • Increased PTEN levels correlated with decreased phosphorylated Akt, indicating PI3K pathway inhibition.

Conclusions:

  • PPARgamma activation upregulates PTEN expression in pancreatic cancer cells.
  • This activation leads to the inhibition of the pro-survival PI3K pathway.
  • Targeting PPARgamma may offer a novel therapeutic strategy for pancreatic cancer.

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