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

Prostaglandins Other Lipid Mediat. 2015 Sep;121(Pt A):42-5. doi: 10.1016/j.prostaglandins.2015.06.006. Epub 2015 Jul 3.

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.

Keywords: 15-Hydroxyprostagladin dehydrogenase; Colon carcinogenesis; Microsomal prostaglandin E synthase-1; Prostaglandin E(2); Prostaglandin E(2) receptor.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

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

Substances

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