Intestinal-specific PPARγ deficiency enhances tumorigenesis in ApcMin/+ mice

Christen A. McAlpine, Yaacov Barak, Ilze Matise, Robert T Cormier

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64 Scopus citations


Multiple investigations of the effects of peroxisome proliferator-activated receptor γ (PPARγ) ligands on colon cancer have produced contradictory results. While some studies demonstrated increased numbers of colonic polyps in ApcMin/+ mice treated with various thiazolidinedione (TZD) PPARγ ligands, others reported amelioration of tumor multiplicity and progression in both ApcMin/+ mice and in mice with chemically-induced colon cancer. Here, we addressed the role of PPARγ in murine intestinal tumorigenesis using gene knockout methodology. We found that either heterozygous or homozygous intestinal-specific PPARγ deficiency enhanced the number of ApcMin/+ tumors in both the small intestine and colon, especially in the colon, where PPARγ deficiency also modulated tumor incidence. Gender significantly affected tumor multiplicity independent of PPARγ genotype. Female ApcMin+ mice developed more tumors in the small intestine and more tumors overall, whereas male ApcMin/+ mice developed more tumors in the colon. Nevertheless, intestinal PPARγ deficiency enhanced tumorigenesis irrespective of gender. Our results suggest that PPARγ functions as a tumor resistance factor in the mouse intestine and warrant further investigation of the PPARγ-dependent and independent actions of TZDs in cancer.

Original languageEnglish (US)
Pages (from-to)2339-2346
Number of pages8
JournalInternational Journal of Cancer
Issue number10
StatePublished - Nov 15 2006


  • Apc
  • Colon cancer
  • Min
  • PPARγ

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