期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 102, 期 51, 页码 18567-18571出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0509316102
关键词
peroxisome proliferator-activated receptor gamma; retinoid X receptor alpha
资金
- NCI NIH HHS [CA81534, U19 CA113318, CA113318, P01 CA081534] Funding Source: Medline
Activation of the Wnt/beta-catenin pathway promotes the development of several cancers and is an attractive target for chemopreventive and chemotherapeutic agents. Nonsteroidal anti-inflammatory drugs (NSAIDs) have been reported to antagonize beta-catenin function, but their mechanism of action is not known. We demonstrate here that interference with beta-catenin function by NSAIDs does not correlate with cyclooxygenase (COX) inhibition. Instead, NSAID inhibition of p-catenin requires the high level expression of peroxisome proliferator-activated receptor gamma (PPAR-gamma) and its co-receptor retinoid-X-receptor alpha (RXR-alpha). Immunciprecipitation experiments show that beta-catenin interacts with RXR-a and PPAR-gamma in some malignant cells. Repression of beta-catenin-dependent transcription by NSAIDs is thus indirect and depends on the coexpression of other nuclear receptors.
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