| Project/Area Number |
12670226
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | NATIONAL CANCER CENTER RESEARCH INSTITUTE |
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Principal Investigator |
KAWAMORI Toshihiko NATIONAL CANCER CENTER RESEARCH INSTITURE, CANCER PREVENTION DIVISION, SECTION HEAD, 研究所・がん予防研究部, 室長 (80311413)
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| Co-Investigator(Kenkyū-buntansha) |
WAKABAYASHI Keiji NATIONAL CANCER CENTER RESEARCH INSTITURE, CANCER PREVENTION DIVISION, CHIEF, 研究所・がん予防研究部, 部長 (60158582)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2000: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | COLON CARCINOGENESIS / PROSTANOIDS / RECEPTOR / KNOCKOUT MICE / ABERRANT CRYPT FOCI / EPI / EP4 / 大腸がん |
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| Research Abstract |
There is accumulating evidence that arachidonic acid cascade is closely related with colon cancer development. Prostanoids, arachidonic acid metabolites, exert their biological functions through binding to their membrane receptors. Eight types of prostanoid receptors have been identified (EP1 4 for PGE2, DP for PGD2, FP for PGF2α, IP for PGI2, and TP for TxA2). Roles of prostanoid receptors in colon carcinogenesis were still unknown. Therefore, we investigated if receptor deficient mice reduced aberrant crypt foci (ACF), thought to be preneoplastic lesions, induced by azoxymethane (AOM). Two types of receptor deficient mice (EP1 and EP4) reduced number of ACF as compared with wild type mice (36 ＆ 44% reduction, respectively). Then, we confirmed the results using selective receptor antagonists. We concluded that EP1 and EP4 receptors play pivotal roles in colon carcinogenesis.
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