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Role of the Prostaglandin E Receptor Subtype EP₁ in Colon Carcinogenesis¹

Cancer Prevention Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan [K. Wat., T. K., S. Nak., T. O., T. S., K. Wak.]; Minase Research Institute, Ono Pharmaceutical Co. Ltd., Osaka 618-8585, Japan [S. O., H. Y., T. M., K. K.]; and Department of Pharmacology, Faculty of Medicine, Kyoto University, Kyoto 606-8315, Japan [F. U., S. Nar.]

Although the cyclooxygenase pathway of the arachidonic acid cascade has been suggested to play an important role in colon carcinogenesis, the molecular species of prostanoids and receptors involved have not been fully elucidated yet. We examined the development of aberrant crypt foci (ACFs), putative preneoplastic lesions of the colon, in two lines of knockout mice, each deficient in prostaglandin E receptors, EP₁ and EP₃, by treatment with the colon carcinogen, azoxymethane. Formation of ACFs was decreased only in the EP₁-knockout mice to 60% of the level in wild-type mice. Administration of 250, 500, or 1000 ppm of a novel selective EP₁ antagonist, ONO-8711, in the diet to azoxymethane-treated C57BL/6J mice also resulted in a dose-dependent reduction of ACF formation. Moreover, when Min mice, having a nonsense mutation in the adenomatous polyposis coli gene, were given 500 ppm ONO-8711 in the diet, the number of intestinal polyps was significantly reduced to 57% of that in the basal diet group. These results strongly suggest that prostaglandin E₂ contributes to colon carcinogenesis to some extent through its action at the EP₁ receptor. Thus, EP₁ antagonists may be good candidates as chemopreventive agents for colon cancer.

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