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- W1569890749 abstract "目的探讨IL-6、IL-8促进卵巢癌细胞增殖的分子机制。方法在以往工作的基础上，选择兼有IL-6、IL-8受体及雄激素受体（androgen receptor，AR）表达的卵巢癌细胞系SKOV-3和OVCAR-3作为研究模型，观察AR阻断剂氟他胺（flutamide，Flu）对IL-6、IL-8诱导的促卵巢癌细胞增殖作用的影响，在此基础上进一步探讨两种细胞因子对AR表达的调节作用及相关信号传导通路。结果①AR阻断剂Flu不能阻断反而增强IL-6、IL-8诱导的促卵巢癌细胞增殖效应。②在无雄激素的条件下，IL-6、IL-8不仅能增加AR表达而且还能活化AR基因启动子，后者可被Flu完全阻断。③IL-6诱导的AR水平增加可被p38MAPK、MEKI／2及ErbB2MAPK阻断剂阻断，而IL-8诱导的AR水平增加则可被Src阻断剂阻断。结论IL-6、IL-8很可能通过提高AR水平和AR活性从而增强卵巢癌细胞对雄激素的敏感性，由此通过产生的放大信号通路促进卵巢癌的生长和发展。IL-6、IL-8的上述活性分别依赖MAPK途径和Src活化。" @default.
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- W1569890749 date "2008-08-31" @default.
- W1569890749 modified "2023-09-23" @default.
- W1569890749 title "IL-6、IL-8上调卵巢癌细胞雄激素受体表达的作用分别依赖MAPK途径和Src活化" @default.
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