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[Cancer Research 66, 6649-6656, July 1, 2006]
© 2006 American Association for Cancer Research

Cell, Tumor, and Stem Cell Biology

Repression of Prostaglandin Dehydrogenase by Epidermal Growth Factor and Snail Increases Prostaglandin E2 and Promotes Cancer Progression

Jason R. Mann1, Michael G. Backlund2, F. Gregory Buchanan2, Taki Daikoku3, Vijaykumar R. Holla2, Daniel W. Rosenberg5, Sudhansu K. Dey3 and Raymond N. DuBois1,2,4

Departments of 1 Cell and Developmental Biology, 2 Medicine, 3 Pediatrics and Pharmacology, and 4 Cancer Biology, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee and 5 Program in Colorectal Cancer, Center for Molecular Medicine, University of Connecticut Health Center, Farmington, Connecticut

Requests for reprints: Raymond N. DuBois, Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, 698 Preston Research Building, 2300 Pierce Avenue, Nashville, TN 37232. Phone: 615-343-0527; Fax: 615-936-2697; E-mail: raymond.dubois{at}vanderbilt.edu.

Prostaglandin E2 (PGE2), a proinflammatory bioactive lipid, promotes cancer progression by modulating proliferation, apoptosis, and angiogenesis. PGE2 is a downstream product of cyclooxygenase (COX) and is biochemically inactivated by prostaglandin dehydrogenase (PGDH). In the present study, we investigated the mechanisms by which PGDH is down-regulated in cancer. We show that epidermal growth factor (EGF) represses PGDH expression in colorectal cancer cells. EGF receptor (EGFR) signaling induces Snail, which binds conserved E-box elements in the PGDH promoter to repress transcription. Induction of PGE2 catabolism through inhibition of EGFR signaling blocks cancer growth in vivo. In human colon cancers, elevated Snail expression correlates well with down-regulation of PGDH. These data indicate that PGDH may serve a tumor suppressor function in colorectal cancer and provide a possible COX-2–independent way to target PGE2 to inhibit cancer progression. (Cancer Res 2006; 66(13): 6649-56)




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Copyright © 2006 by the American Association for Cancer Research.