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Lookup NU author(s): Dr Kelly Coffey,
Professor Craig Robson,
Professor Hing Leung
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BACKGROUND. Fibroblast growth factor 8 (FGF8) is over-expressed in prostate cancer (CaP) correlating with high-grade disease and reduced survival. The role of acetylation in transcriptional regulation of FGF8 was investigated using the histone deacetylase (HDAC) inhibitor Trichostatin A (TSA). METHODS. FGF8 transcriptional response to TSA was investigated by gene reporter assays, RT-PCR, and Western blotting. Chromatin immunoprecipitation (ChIP) assays were also performed. RESULTS. FGF8 is upregulated in response to TSA treatment along with NF-κB transcriptional activity. Over-expression of p65 activated FGF8 transcription. ChIP assays revealed p65 recruitment to the/g/8 promoter, containing putative NF-κB binding sites, post TSA stimulation. P1-3K activity is required for TSA mediated FGF8 upregulation. CONCLUSION. Using TSA treatment in prostate cancer cells, a requirement of PI-3K activity in mediating TSA function is demonstrated and a novel role for NF-κB in the regulation of FGF8 expression is uncovered. © 2006 Wiley-Liss. Inc.
Author(s): Armstrong K, Robson CN, Leung HY
Publication type: Article
Publication status: Published
Journal: The Prostate
Print publication date: 01/08/2006
ISSN (print): 0270-4137
ISSN (electronic): 1097-0045
PubMed id: 16683270
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