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Carcinogenesis Advance Access originally published online on November 25, 2004
Carcinogenesis 2005 26(2):353-357; doi:10.1093/carcin/bgh322
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Carcinogenesis vol.26 no.2 © Oxford University Press 2005; all rights reserved.

ARTICLE

Prostaglandin E receptor subtype EP1 deficiency inhibits colon cancer development

Toshihiko Kawamori3, Tomohiro Kitamura, Kouji Watanabe, Naoaki Uchiya, Takayuki Maruyama1, Shuh Narumiya2, Takashi Sugimura and Keiji Wakabayashi*

Cancer Prevention Basic Research Project, National Cancer Center Research Institute, 1-1 Tsukiji 5-chome, Chuo-ku, Tokyo 104-0045, Japan, 1 Minase Research Institute, Ono Pharmaceutical Co. Ltd, Osaka 618-8585, Japan and 2 Department of Pharmacology, Faculty of Medicine, Kyoto University, Kyoto 606-8315, Japan

* To whom correspondence should be addressed Email: kawamori{at}musc.edu or kwakabay{at}gan2.ncc.go.jp

Prostaglandin E2 exerts its biological activity through binding to its membrane receptors, E-prostanoid (EP) receptors1–4. Our previous finding that lack of EP1 receptor inhibits the early stages of colon carcinogenesis led us to investigate whether EP1 receptor deficiency reduces colon cancer development induced by azoxymethane (AOM) using EP1 receptor knockout mice. At 6 weeks of age 33 homozygous EP1-deficient (EP1–/–) mice and 28 wild-type (EP1+/+) mice were given i.p. AOM (10 mg/kg body wt) once a week for 6 weeks. At 56 weeks of age all animals were killed and intestinal tumors were examined. The results clearly indicated that lack of EP1 receptor significantly reduced colon cancer incidence (27 versus 57%, P < 0.05) and multiplicity (0.30 versus 0.76, P < 0.05) as well as tumor volume (12.2 versus 75.6 mm3, P < 0.05). In EP1–/– mice, silver stained nucleolar organization region protein count as cell proliferation marker was significantly reduced (1.35 versus 2.17, P < 0.001) and apoptosis was significantly increased (0.685 versus 0.077, P < 0.001) in colon tumors induced by AOM compared with those in EP1+/+ mice. We confirmed that EP1 receptor mRNA was overexpressed in colon cancers of EP1+/+ mice using reverse transcription–polymerase chain reaction. These results provide strong evidence that the EP1 receptor is of major importance for colon cancer development and it could be a new target for a mechanism-based chemoprevention strategy against colon cancer development.


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