期刊
FEBS LETTERS
卷 579, 期 20, 页码 4213-4218出版社
WILEY
DOI: 10.1016/j.febslet.2005.06.049
关键词
Wnt/beta-catenin signaling; nuclear factor-kappa B; diclofenac; colon cancer cell
The dysregulation of Wnt/beta-catenin signaling and subsequent upregulation of beta-catenin response transcription (CRT) occur frequently in colon cancer cells. Non-steroidal anti-inflammatory drugs (NSAIDs) can repress CRT in colorectal cancer, but little is known about the mechanism of action. We show that the NSAID diclofenac inhibits Wnt/beta-catenin signaling without altering the level of beta-catenin protein and reduces the expression of beta-catenin/TCF-dependent genes. Diclofenac induced the degradation of I kappa B alpha, which increased free nuclear factor kappa B (NF-kappa B) in cells. Also, the ectopic expression of p65, which is a component of NF-kappa B, suppressed CRT. Our findings suggest that diclofenac inhibits Wnt/beta-catenin signaling via the activation of NF-kappa B in colon cancer cells. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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