PPAR delta status and Apc-mediated tumourigenesis in the mouse intestine

Reed, K., Sansom, O. , Hayes, A., Gescher, A., Winton, D., Peters, J. and Clarke, A. (2004) PPAR delta status and Apc-mediated tumourigenesis in the mouse intestine. Oncogene, 23, pp. 8992-8996. (doi:10.1038/sj.onc.1208143)

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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 Apc(Min)PPARdelta-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.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Sansom, Professor Owen
Authors: Reed, K., Sansom, O., Hayes, A., Gescher, A., Winton, D., Peters, J., and Clarke, A.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cancer Sciences
Journal Name:Oncogene
ISSN:0950-9232

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