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Originally published In Press as doi:10.1074/jbc.M210707200 on October 21, 2002

J. Biol. Chem., Vol. 277, Issue 52, 50828-50833, December 27, 2002
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Autocrine/Paracrine Prostaglandin E2 Production by Non-small Cell Lung Cancer Cells Regulates Matrix Metalloproteinase-2 and CD44 in Cyclooxygenase-2-dependent Invasion*

Mariam DohadwalaDagger §, Raj K. BatraDagger §, Jie LuoDagger , Ying LinDagger , Kostyantyn KrysanDagger , Mehis PõldDagger , Sherven SharmaDagger §, and Steven M. DubinettDagger §||

From the  Lung Cancer Research Program of the UCLA Jonsson Comprehensive Cancer Center and Dagger  Division of Pulmonary and Critical Care Medicine, Departments of Medicine, David Geffen School of Medicine at UCLA and the § Veterans Affairs Greater Los Angeles Health Care Center, Los Angeles, California 90095

Tumor cyclooxygenase-2 (COX-2) expression is known to be associated with enhanced tumor invasiveness. In the present study, we evaluated the importance of the COX-2 product prostaglandin E2 (PGE2) and its signaling through the EP4 receptor in mediating non-small cell lung cancer (NSCLC) invasiveness. Genetic inhibition of tumor COX-2 led to diminished matrix metalloproteinase (MMP)-2, CD44, and EP4 receptor expression and invasion. Treatment of NSCLC cells with exogenous 16,16-dimethylprostaglandin E2 significantly increased EP4 receptor, CD44, and MMP-2 expression and matrigel invasion. In contrast, anti-PGE2 decreased EP4 receptor, CD44, and MMP-2 expression in NSCLC cells. EP4 receptor signaling was found to be central to this process, because antisense oligonucleotide-mediated inhibition of tumor cell EP4 receptors significantly decreased CD44 expression. In addition, agents that increased intracellular cAMP, as is typical of EP4 receptor signaling, markedly increased CD44 expression. Moreover, MMP-2-AS treatment decreased PGE2-mediated CD44 expression, and CD44-AS treatment decreased MMP-2 expression. Thus, PGE2-mediated effects through EP4 required the parallel induction of both CD44 and MMP-2 expression because genetic inhibition of either MMP-2 or CD44 expression effectively blocked PGE2-mediated invasion in NSCLC. These findings indicate that PGE2 regulates COX-2-dependent, CD44- and MMP-2-mediated invasion in NSCLC in an autocrine/paracrine manner via EP receptor signaling. Thus, blocking PGE2 production or activity by genetic or pharmacological interventions may prove to be beneficial in chemoprevention or treatment of NSCLC.

* This work was supported by National Institutes of Health Grants P50 CA90388 and RO1 CA71818, the American Lung Association, Merit Review Research Funds from the Department of Veterans Affairs, the Tobacco-related Disease Research Program of the University of California, and the Research Enhancement Award Program in Cancer Gene Medicine.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.

|| To whom correspondence and reprint requests should be addressed: David Geffen School of Medicine at UCLA, 37-131 CHS, 10833 Le Conte Ave., Los Angeles, CA 90095. Tel.: 310-794-6566; Fax: 310-267-2829; E-mail: sdubinett@mednet.ucla.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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