Journal Article

Suppression of cyclooxygenase-2 promoter-dependent transcriptional activity in colon cancer cells by chemopreventive agents with a resorcin-type structure

Michihiro Mutoh, Mami Takahashi, Kazunori Fukuda, Yuko Matsushima-Hibiya, Hiroshi Mutoh, Takashi Sugimura and Keiji Wakabayashi

in Carcinogenesis

Volume 21, issue 5, pages 959-963
Published in print May 2000 | ISSN: 0143-3334
Published online May 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.5.959
Suppression of cyclooxygenase-2 promoter-dependent transcriptional activity in colon cancer cells by chemopreventive agents with a resorcin-type structure

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Cyclooxygenase-2 (COX-2) is abundantly expressed in colon cancer cells. It has been reported that inhibition of COX-2 enzyme activity is shown to prevent colon carcinogenesis. Thus, suppression of COX-2 expression may also be an effective chemopreventive strategy. In the present study, we constructed a β-galactosidase reporter gene system in human colon cancer DLD-1 cells, and measured COX-2 promoter-dependent transcriptional activity in the cells. Interferon γ suppressed this COX-2 promoter activity, while 12-O-tetradecanoylphorbol-13-acetate and transforming growth factor α (TGFα) exerted enhancing effects. We then tested the influence of 14 candidate cancer chemopreventive compounds on COX-2 promoter activity. Chemopreventive agents such as quercetin, kaempferol, genistein, resveratrol and resorcinol, all having a common resorcin moiety, were found to effectively suppress the COX-2 promoter activity with and without TGFα-stimulation in DLD-1 cells. Since all these compounds have a resorcin moiety as a common structure, a resorcin-type structure may play an active role in the inhibition of COX-2 expression in colon cancer cells.

Keywords: β-gal, β-galactosidase; COX, cyclooxygenase; DHA, docosahexaenoic acid; FBS, fetal bovine serum; IFNγ, interferon γ; IL, interleukin; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; NSAIDs, non-steroidal anti-inflammatory drugs; TGFα, transforming growth factor α; TPA, 12-O-tetradecanoylphorbol-13-acetate; PTKs, protein-tyrosine kinases.

Journal Article.  3751 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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