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The Wnt/beta-catenin signaling pathway targets PPARgamma activity in colon cancer cells

Emmelie A Jansson1, Alexandra Are, Gediminas Greicius

  • 1Microbiology and Tumor Biology Center, Karolinska Institutet, S-17177 Stockholm, Sweden.

Proceedings of the National Academy of Sciences of the United States of America
|January 25, 2005
PubMed

Insights

Aberrant Wnt/beta-catenin signaling disrupts colon cell fate in cancer. Peroxisome proliferator-activated receptor-gamma (PPARgamma) interacts with beta-catenin, influencing cell fate and acting as a Wnt pathway target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Colon cell fate control is disrupted in adenocarcinomas by aberrant Wnt/beta-catenin signaling.
  • Peroxisome proliferator-activated receptor-gamma (PPARgamma) is implicated in colon cancer development.
  • PPARgamma expression is altered in the APCMin mouse model of colon cancer.

Purpose of the Study:

  • To investigate the role of PPARgamma in colon cancer.
  • To explore the relationship between Wnt/beta-catenin signaling and PPARgamma levels.
  • To elucidate the mechanism by which PPARgamma influences colon cancer cell fate.

Main Methods:

  • Analysis of PPARgamma expression in the APCMin mouse model.
  • Investigation of PPARgamma protein levels in colon cancer cell lines.
  • Induction of Wnt/beta-catenin pathway using LiCl and assessment of PPARgamma activity.
  • Examination of interactions between PPARgamma, beta-catenin, and Tcf-4.

Main Results:

  • PPARgamma protein levels are elevated in colon cancer cells, potentially due to sequestration by activated beta-catenin.
  • Wnt/beta-catenin pathway induction elevates PPARgamma levels and activates PPARgamma-dependent genes.
  • PPARgamma interacts with beta-catenin and Tcf-4, suggesting a role in cell fate determination.

Conclusions:

  • PPARgamma is a target of the Wnt pathway in colon cancer cells.
  • PPARgamma, through interactions with beta-catenin and Tcf-4, may determine colon cancer cell fate.
  • Aberrant Wnt/beta-catenin signaling and altered PPARgamma contribute to colon adenocarcinoma development.

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