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[Cancer Research 62, 28-32, January 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Involvement of Prostaglandin E Receptor Subtype EP4 in Colon Carcinogenesis1

Michihiro Mutoh2, Kouji Watanabe2, Tomohiro Kitamura, Yutaka Shoji, Mami Takahashi, Toshihiko Kawamori, Kousuke Tani, Michiyoshi Kobayashi, Takayuki Maruyama, Kaoru Kobayashi, Shuichi Ohuchida, Yukihiko Sugimoto, Shuh Narumiya, Takashi Sugimura and Keiji Wakabayashi3

Cancer Prevention Division, National Cancer Center Research Institute, Tokyo 104-0045, Japan [M. M., K. Wat., T. Kit., Y. S., M. T., T. Kaw., T. S., K. Wak.]; Minase Research Institute, Ono Pharmaceutical Co. Ltd., Osaka 618-8585, Japan [K. T., M. K., T. M., K. K., S. O.]; Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Kyoto University, Kyoto 606-8315, Japan [Y. S.]; and Department of Pharmacology, Faculty of Medicine, Kyoto University, Kyoto 606-8315, Japan [S. N.]

Accumulating evidence indicates that overproduction of prostanoids attributable to overexpression of cyclooxygenase-2 (COX-2) plays an important role in colon carcinogenesis. We have shown recently that the prostaglandin (PG) E receptor, EP1, but not EP3, is involved in mouse colon carcinogenesis. In line with our previous study, here we examined the role of prostanoid receptors in colon carcinogenesis using six additional lines of knockout mice deficient in prostanoid receptors EP2, EP4, DP, FP, IP, or TP. The animals were treated with the colon carcinogen, azoxymethane (AOM), and examined for the development of aberrant crypt foci (ACFs), putative preneoplastic lesions in the colon. Formation of ACFs was decreased only in the EP4-knockout mice, to 56% of the wild-type level. To confirm these results, we also examined the inhibitory effects of an EP4-selective antagonist, ONO-AE2-227, in the diet on the formation of AOM-induced colon ACFs in C57BL/6Cr mice and on the development of intestinal polyps in Min mice. ONO-AE2-227 at a dose of 400 ppm reduced the formation of ACFs to 67% of the control level, and intestinal polyp numbers in Min mice receiving 300 ppm were decreased to 69% of the control level. Plating efficiency assays showed that addition of 1.0 µM ONO-AE1-329, an EP4-selective agonist, resulted in a 1.8-fold increase in the colony number of the human colon cancer cell line, HCA-7, similar to the effect of PGE2. Moreover, EP4 mRNA expression was clearly observed in normal colon mucosa and colon tumors in mice. Our previous and present results indicate that PGE2 contributes to colon carcinogenesis through its actions mediated through EP1 and EP4 receptors; therefore, antagonists for these two receptors may be good candidates as chemopreventive agents against colon cancer.




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