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Originally published In Press as doi:10.1074/jbc.C100339200 on November 1, 2001

J. Biol. Chem., Vol. 276, Issue 50, 47131-47135, December 14, 2001
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Early de Novo Gene Expression Is Required for 15-Deoxy-Delta 12,14-prostaglandin J2-induced Apoptosis in Breast Cancer Cells*

Carl E. ClayDagger §, Gen-ichi AtsumiDagger §||, Kevin P. HighDagger ||**, and Floyd H. ChiltonDagger §Dagger Dagger

From the Dagger  Department of Internal Medicine, § Section of Pulmonary Critical Care, || Section of Infectious Diseases, and Dagger Dagger  Department of Physiology and Pharmacology, Wake Forest University Baptist Medical Center, Winston Salem, North Carolina 27157

Cyclopentenone prostaglandin derivatives of arachidonic acid are potent inducers of apoptosis in a variety of cancer cell types. Several investigators have shown that the terminal derivative of prostaglandin J2 (PGJ2) metabolism, 15-deoxy-Delta 12,14-PGJ2 (15dPGJ2), induces apoptosis in breast cancer cells and is a potent activator of the nuclear hormone receptor peroxisome proliferator-activated receptor gamma  (PPARgamma ), but 15dPGJ2 effects can be mediated by PPARgamma -dependent and PPARgamma -independent mechanisms. Here we report that 15dPGJ2 regulates early gene expression critical to apoptosis. Specifically, 15dPGJ2 induces potent and irreversible S phase arrest that is correlated with expression of genes critical to cell cycle arrest and apoptosis, including the cyclin-dependent kinase inhibitor p21Waf1/Cip1 (p21). Inhibition of RNA or protein synthesis abrogates apoptosis induced by 15dPGJ2 in breast cancer cells but potentiates apoptosis induced by tumor necrosis factor-alpha or CD95/Fas ligand. Additionally, 15dPGJ2 induces caspase activation that is blocked by peptide caspase inhibitors. These data show that de novo gene transcription is necessary for 15dPGJ2-induced apoptosis in breast cancer cells. Critical candidate genes are likely to be revealed through analysis of differential cDNA array expression.

* This work was supported by National Institutes of Health Grant RO1AI42022 and American Institute of Cancer Research Grant 97B108.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received support through Grant DAMD17-00-1-0489 from the United States Army Medical Research Acquisition Activity (USAMRAA).

** To whom correspondence should be addressed: Dept. of Internal Medicine, Section of Infectious Diseases, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1042. Tel.: 336-716-4584; Fax: 336-716-3825; E-mail: khigh@wfubmc.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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