期刊
PROSTATE
卷 66, 期 11, 页码 1223-1234出版社
WILEY
DOI: 10.1002/pros.20376
关键词
HDAC; trichostatin A; PI-3K; FGF8; prostate
资金
- Medical Research Council [G0100100] Funding Source: Medline
- MRC [G0100100] Funding Source: UKRI
- Medical Research Council [G0100100] Funding Source: researchfish
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-kappa B transcriptional activity. Over-expression of p65 activated FGF8 transcription. ChIP assays revealed p65 recruitment to the fgf8 promoter, containing putative NF-kappa B binding sites, post TSA stimulation. PI-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-kappa B in the regulation of FGF8 expression is uncovered.
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