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首页> 外文期刊>Cancer Cell >Enhanced paracrine FGF10 expression promotes formation of multifocal prostate adenocarcinoma and an increase in epithelial androgen receptor.
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Enhanced paracrine FGF10 expression promotes formation of multifocal prostate adenocarcinoma and an increase in epithelial androgen receptor.

机译:旁分泌FGF10表达的增强促进了多灶性前列腺腺癌的形成和上皮雄激素受体的增加。

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摘要

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 FGF10-induced carcinoma was serially transplantable. Paracrine FGF10 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 FGF10/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.
机译:FGF10的间充质表达增强导致多灶性PIN或前列腺癌的形成。使用DN FGFR1抑制上皮FGFR1信号传导会导致癌症表型的逆转。 FGF10诱导的癌的一个子集可以串行移植。旁分泌FGF10导致上皮雄激素受体增加,并与细胞自主激活的AKT协同作用。我们的观察结果表明基质FGF10表达可能促进在前列腺腺癌中观察到的多灶性组织学,并提示FGF10 / FGFR1轴是治疗激素敏感性或难治性前列腺癌的潜在治疗靶标。我们还表明,短暂暴露于旁分泌生长因子可能足以引发致癌转化。

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