Role of microsomal prostaglandin E synthase-1 (mPGES-1)-derived prostaglandin E2 in colon carcinogenesis.

Abstract

Nonsteroidal anti-inflammatory drugs, especially selective cyclooxygenase-2 (COX-2) inhibitors, are among the most promising chemopreventive agents for colorectal cancer. However, recent clinical trials have indicated that these inhibitors pose a significantly increased cardiovascular risk. Microsomal prostaglandin E (PGE) synthase-1 (mPGES-1) and mPGES-1-derived PGE2 have gained attention recently as alternative targets to COX-2 for colorectal cancer chemoprevention and chemotherapy. In this review, we summarize the current understanding of the roles of mPGES-1, a PGE2-inactivating enzyme (15-hydroxyprostagladin dehydrogenase), and PGE2 specific receptors (EPs) in colon carcinogenesis.

• Authors: Yuka Sasaki, Yoshihito Nakatani, Shuntaro Hara
• Journal: Prostaglandins & other lipid mediators (Prostaglandins Other Lipid Mediat) Vol. 121 Issue Pt A Pg. 42-5 (Sep 2015) ISSN: 1098-8823 [Print] United States
• PMID: 26150361 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2015 Elsevier Inc. All rights reserved.

Chemical References

• Receptors, Prostaglandin E
• Hydroxyprostaglandin Dehydrogenases
• 15-hydroxyprostaglandin dehydrogenase
• Dinoprostone

Topics

• Animals
• Carcinogenesis
• Colonic Neoplasms (enzymology, metabolism, pathology)
• Dinoprostone (metabolism)
• Humans
• Hydroxyprostaglandin Dehydrogenases (metabolism)
• Receptors, Prostaglandin E (metabolism)