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Carcinogenesis Advance Access originally published online on March 28, 2003
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Carcinogenesis, Vol. 24, No. 5, 985-990, May 2003
© 2003 Oxford University Press

CARCINOGENESIS

Enhancement of colon carcinogenesis by prostaglandin E2 administration

Toshihiko Kawamori1, Naoaki Uchiya, Takashi Sugimura and Keiji Wakabayashi2

Cancer Prevention Division, National Cancer Center Research Institute, 1-1 Tsukiji 5-chome, Chuo-ku, Tokyo 104-0045, Japan

2 To whom correspondence should be addressed Email: kwakabay{at}gan2.res.ncc.go.jp

Although an accumulating body of evidence indicates that levels of prostaglandin E2 (PGE2) in human and rodent colon cancers are higher than those in surrounding normal tissues, the precise contribution of PGE2 to the process of colon cancer development has still been unclear. Therefore, we designed a study using a well-established azoxymethane (AOM)-induced colon carcinogenesis in male F344 rat model to investigate whether administration of exogenous PGE2 has a real impact on colon carcinogenesis. Intraperitoneal PGE2 injections (7.7 µg) once a week for 25 weeks significantly increased the AOM-induced colon tumor incidence (percent rats with tumors, 92 versus 53%, P < 0.05), especially adenocarcinomas (92 versus 47%, P < 0.05), and multiplicity (number of tumors per rat, 2.8 versus 1.0, P < 0.05). PGE2 treatment significantly increased 5-bromo-2'-deoxyuridine (BrdUrd) labeling index (11.8 versus 9.7%, P < 0.05) and reduced apoptotic index (0.34 versus 0.53%, P < 0.05) in colon cancers induced by AOM. PGE2 exhibits its physiological functions through binding to E-prostanoid (EP) membrane receptors EP1-4. All four types of EP receptors were detected in AOM-induced colon cancers using reverse transcription–polymerase chain reaction (RT–PCR). Our results provide evidence that PGE2 enhances colon carcinogenesis through induction of cell proliferation and reduction of apoptosis.


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