PPARδ Is an APC-Regulated Target of Nonsteroidal Anti-Inflammatory Drugs
作者： Tong-Chuan He , Timothy A Chan , Bert Vogelstein , Kenneth W Kinzler , None
DOI: 10.1016/S0092-8674(00)81664-5
关键词: Psychological repression 、 Beta-catenin 、 Gene expression 、 Carcinogenesis 、 Regulation of gene expression 、 Transcription factor 、 Receptor 、 Biology 、 Pharmacology 、 Sulindac
摘要: PPARB was identified as a target of APC through the analysis global gene expression profiles in human colorectal cancer (CRC) cells. PPARdelta elevated CRCs and repressed by CRC This repression mediated beta-catenin/Tcf-4-responsive elements promotor. The ability PPARs to bind eicosanoids suggested that might be chemopreventive non-steroidal anti-inflammatory drugs (NSAIDs). Reporters containing PPARdelta-responsive were NSAID sulindac. Furthermore, sulindac able disrupt its recognition sequences. These findings suggest NSAIDs inhibit tumorigenesis inhibition PPARdelta, for which is normally regulated APC.
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