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J. Lipid Res.
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A more recent version of this article appeared on November 1, 2002

Papers In Press, published online ahead of print August 16, 2002
J. Lipid Res., doi:10.1194/jlr.M200224-JLR200
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Submitted on June 8, 2002
Revised on July 24, 2002
Accepted on August 6, 2002

15-Deoxy-D12,14-prostaglandin J2-induced apoptosis does not require PPARg in breast cancer cells

Carl E. Clay, Arta M. Monjazeb, Jacqueline Thorburn, Floyd H. Chilton, and Kevin P. High

Medicine, Washington University School of Medicine, St. Louis, MO 63110

Corresponding Author: cclay{at}im.wustl.edu

Naturally occurring derivatives of arachidonic acid are potent agonists for the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARg) and block cancer cell proliferation through the induction of apoptosis. We have previously reported that induction of apoptosis using cyclopentenone prostaglandins of the J series, including 15deoxyD12,14PGJ2 (15dPGJ2), is associated with a high degree of PPAR-response element (PPRE) activity and requires early de novo gene expression in breast cancer cells. In the current study, we used pharmacologic and genetic approaches to test the hypothesis that PPARg is required for 15dPGJ2-induced apoptosis. The PPARg agonists 15dPGJ2, trogliltazone (TGZ) and GW7845, a synthetic and highly selective tyrosine-based PPARg agonist, all increased transcriptional activity of PPARg, and expression of CD36, a PPARg-dependent gene. Transcriptional activity and CD36 expression was reduced by GW9662, a selective and irreversible PPARg antagonist, but GW9662 did not block apoptosis induced by 15dPGJ2. Moreover, dominant negative expression of PPARg blocked PPRE transcriptional activity, but did not block 15dPGJ2-induced apoptosis. These studies show that while 15dPGJ2 activates PPRE-mediated transcription, PPARg is not required for 15dPGJ2-induced apoptosis in breast cancer cells. Other likely mechanisms through which cyclopentenone prostaglandins induce apoptosis of cancer cells are discussed.


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