期刊
CANCER CELL
卷 12, 期 6, 页码 572-585出版社
CELL PRESS
DOI: 10.1016/j.ccr.2007.11.002
关键词
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资金
- Howard Hughes Medical Institute Funding Source: Medline
- NCI NIH HHS [R01 CA107166, R01CA90571, R01CA107300, K12 CA076905, K12-CA076905-09, R01 CA090571, 1K99CA125937, R01 CA107300, K99 CA125937] Funding Source: Medline
- NICHD NIH HHS [K12 HD000849, 5K12HD00849-18, K12 HD000849-18] Funding Source: Medline
Enhanced mesenchymal expression of FGF10 led to the formation of multifocal PIN or prostate cancer. Inhibition of epithelial FGFR1 signaling using DN FGFR1 led to reversal of the cancer phenotype. A subset of the FGH10-induced carcinoma was serially transplantable. Paracrine FGH10 led to an increase in epithelial androgen receptor and synergized with cell-autonomous activated AKT. Our observations indicate that stromal FGF10 expression may facilitate the multifocal histology observed in prostate adenocarcinoma and suggest the FGH10/FGFR1 axis as a potential therapeutic target in treating hormone-sensitive or refractory prostate cancer. We also show that transient exposure to a paracrine growth factor may be sufficient for the initiation of oncogenic transformation.
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