Selective PGE(2) suppression inhibits colon carcinogenesis and modifies local mucosal immunity.

ABSTRACT: Prostaglandin E(2) (PGE(2)) is a bioactive lipid that mediates a wide range of physiologic effects and plays a central role in inflammation and cancer. PGE(2) is generated from arachidonic acid by the sequential actions of the COX and terminal synthases (PGES). Increased levels of COX-2, with a concomitant elevation of PGE(2), are often found in colorectal cancers (CRC), providing the rationale for the use of COX-2 inhibitors for chemoprevention. Despite their proven efficacy in cancer prevention, however, COX-2 inhibitors exhibit dose-dependent toxicities that are mediated in part by their nonspecific reduction of essential prostanoids, thus limiting their chemopreventive benefit. To achieve enhanced specificity, recent efforts have been directed toward targeting the inducible terminal sy

SUBMITTER: Nakanishi M 

PROVIDER: S-EPMC3151318 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature