Cox-2, Prostaglandins, And Colon Cancer (pp. 123-141)
Authors: Ota, Shinichi; Bamba, Hiromi; (Saitama Medical School; Saitama, Japan)
Abstract: Epidemiological, experimental, and clinical studies have demonstrated that colon carcinogenesis might be prevented by nonsteroidal anti-inflammatory drug (NSAID). Although there are some controversies, recent studies have revealed that NSAID suppresses colon carcinogenesis at adenoma stage where cyclooxygenase-2, a major molecular target in this action, is mainly expressed in interstitial cells but not in tumor cells. Therefore, it is unlikely that NSAID prevents colon cancer formation through modulating the functions of tumor cells. A more possible assumption is that NSAID suppresses colon carcinogenesis through the inhibition of prostaglandin formation. However, at present mechanisms by which how prostaglandins promote colon carcinogenesis have not been elucidated yet. Since prostaglandins act through both membrane receptors and nuclear receptors such as peroxisome proliferator receptor ã or ä, one of the focus in this area is to investigate their roles in colon carcinogenesis.