PPARδ status and Apc-mediated tumourigenesis in the mouse intestine

Karen R. Reed, Owen J. Sansom, Anthony J. Hayes, Andreas J. Gescher, Douglas J. Winton, Jeffrey M. Peters, Alan R. Clarke

Research output: Contribution to journalArticle

97 Scopus citations

Abstract

Based on recent reports that peroxisome proliferator-activated receptor delta (PPARδ) activation promotes tumourigenesis, we have investigated the role of this protein in Apc-mediated intestinal tumourigenesis. We demonstrate that the inactivation of Apc in the adult small intestine, while causing the expected nuclear accumulation of β-catenin, does not cause the expected increase in PPARδ mRNA or protein but conversely, the levels of PPARδ mRNA and protein are lowered. Furthermore, we find that Apc MinPPARδ-null mice exhibit an increased predisposition to intestinal tumourigenesis. Our data suggest that PPARδ is not directly regulated by β-catenin, and that inhibition of PPARδ activity is unlikely to be an appropriate strategy for the chemoprevention or chemotherapy of intestinal malignancies.

Original languageEnglish (US)
Pages (from-to)8992-8996
Number of pages5
JournalOncogene
Volume23
Issue number55
DOIs
StatePublished - Nov 25 2004

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Cancer Research

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    Reed, K. R., Sansom, O. J., Hayes, A. J., Gescher, A. J., Winton, D. J., Peters, J. M., & Clarke, A. R. (2004). PPARδ status and Apc-mediated tumourigenesis in the mouse intestine. Oncogene, 23(55), 8992-8996. https://doi.org/10.1038/sj.onc.1208143