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

First Author  Reed KR Year  2004
Journal  Oncogene Volume  23
Issue  55 Pages  8992-6
PubMed ID  15480419 Mgi Jnum  J:94711
Mgi Id  MGI:3513724 Doi  10.1038/sj.onc.1208143
Citation  Reed KR, et al. (2004) PPARdelta status and Apc-mediated tumourigenesis in the mouse intestine. Oncogene 23(55):8992-6
abstractText  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.
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