IngentaConnect COX-2, prostanoids and colon cancer

Authors: Ota, S.¹; Bamba, H.¹; Kato, A.²; Kawamoto, C.²; Yoshida, Y.²; Fujiwara, K.¹

Source: Alimentary Pharmacology & Therapeutics, Volume 16, Supplement 2, April 2002 , pp. 102-106(5)

Abstract:

Epidemiological, experimental, and clinical studies have demonstrated that colon carcinogenesis may be prevented by nonsteroidal anti-inflammatory drugs (NSAIDs). Although controversy remains, recent studies, including ours, have revealed that NSAIDs suppress colon carcinogenesis at the adenoma stage where cyclooxygenase-2 (COX-2), a major molecular target in this action, is mainly expressed in interstitial cells but not in tumour cells. Therefore, it is unlikely that NSAIDs prevent colon cancer formation through modulating the functions of tumour cells. A more possible assumption is that NSAIDs suppress colon carcinogenesis through the inhibition of prostaglandin formation. However, the mechanisms by which prostanoids promote colon carcinogenesis have not been elucidated to date. A prostanoids act through both membrane receptors and nuclear receptors such as peroxisome proliferator receptor (PPAR) γ or δ, one focus in this area is to investigate their roles in colon carcinogenesis, including the induction of growth factors.

Document Type: Research article

DOI: 10.1046/j.1365-2036.16.s2.8.x

Affiliations: 1: Third Department of Internal Medicine, Saitama Medical School, Saitama, Japan, 2: First Department of Internal Medicine, Saitama Medical Center, Saitama, Medical School, Saitama, Japan

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