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    Oncogene. 2004 Nov 25;23(55):8992-6.

    PPARdelta status and Apc-mediated tumourigenesis in the mouse intestine.

    Reed KR, Sansom OJ, Hayes AJ, Gescher AJ, Winton DJ, Peters JM, Clarke AR.

    Source

    Cardiff School of Biosciences, Cardiff University, Museum Avenue, Cardiff CF103US, UK.

    Abstract

    Based on recent reports that peroxisome proliferator-activated receptor delta (PPARdelta) 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 beta-catenin, does not cause the expected increase in PPARdelta mRNA or protein but conversely, the levels of PPARdelta mRNA and protein are lowered. Furthermore, we find that ApcMinPPARdelta-null mice exhibit an increased predisposition to intestinal tumourigenesis. Our data suggest that PPARdelta is not directly regulated by beta-catenin, and that inhibition of PPARdelta activity is unlikely to be an appropriate strategy for the chemoprevention or chemotherapy of intestinal malignancies.

    PMID:
    15480419
    [PubMed - indexed for MEDLINE]

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