Prostaglandins (PGs) are lipid mediators and modulate diverse biological and (patho)-physiological processes, such as inflammation and carcinogenesis. Roles of PGs in inflammation and carcinogenesis were provided by pharmacological action of nonsteroidal anti-inflammatory drugs (NSAIDs). In gastrointestinal disease, NSAIDs induce gastric ulcer, exacerbate inflammatory bowl disease (IBD) and reduce adenomatous polyps in patients with familial adenomatous polyposis (FAP). These damaging effects occur principally because of inhibition of PGs synthesis by NSAIDs. Moreover, the selective inhibitor of inducible cyclooxygenase (prostaglandin synthetase, COX-2) exacerbate IBD and reduce adenomatous polyps in patients with FAP. Therefore, these pathophysiological processes may be associated with COX-2 expression. In the past decade, more progress has been made in understanding the role of COX, PGs and PG receptors in biology and diseases. I would like to review the evidence and possible roles of PGs in gastrointestinal disease including colon and gastric cancer.
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