表皮生长因子通过其受体途径诱导小鼠黑素瘤B16细胞迁移的研究  

Mouse melanoma B16 cells migration induced by epidermal growth factor through EGFR/ERK pathways

作　　者：喻丽婷[1] 纪超[1] 毕志刚[1] 张美华[1] 

机构地区：[1]南京医科大学第一附属医院皮肤性病科,江苏南京210029

出　　处：《临床皮肤科杂志》2010年第5期271-274,共4页Journal of Clinical Dermatology

摘　　要：目的:研究表皮生长因子(epidermal growth factor,EGF)诱导小鼠黑素瘤B16细胞移行及其信号通路机制。方法:蛋白质免疫印迹方法分析各蛋白的表达;细胞迁移试验(phagokinetic track motility)测定法观察细胞的迁移。结果:EGF可诱导表皮生长因子受体(EGFR)和细胞外信号调节激酶(ERK)磷酸化,EGF处理后5 min,EGFR和ERK的磷酸化达到峰值,EGFR激酶抑制剂(PD153035)和ERK抑制剂(U0126)可阻断EGF诱导的ERK磷酸化;EGF可显著提高细胞中水通道蛋白-3(aquaporins-3,AQP3)的活性,并随时间延长活性增强,24 h达到较高水平,AQP3活性亦随浓度升高而增强,当EGF浓度为100μg/L时达到较高水平:PD153035、U0126和CuSO_4可抑制AQP3的活性以及细胞的移行。结论:在小鼠黑素瘤B16细胞中,EGF通过磷酸化EGFR,激活ERK,进而使AQP3表达上调,促进B16细胞迁移。这一通路可被EGFR激酶抑制剂、ERK和AQP3抑制剂阻断,这些涉及的信号通路可能形成潜在的治疗黑素瘤的靶点。Objective： To investigate the migration induced by epidermal growth factor （EGF） and its signal pathway in cultured mouse melanoma B16 cells. Methods：Cultured B16 cells were treated with EGF and/or various reagents and subjected to cell migration assay by phagokinetic track motility or biochemical analysis for expression or activation of proteins by SDS-PAGE/Westem blot analysis. Results：Aquaporins-3 （AQP3） was expressed in cultured mouse melanoma B16 cells. AQP3 expression and migration were up-regulated by EGF. EGF-induced cell migration was inhibited by AQP3 water transport inhibitor CuSO_4, and the effects of EGF mediated, at least in part, by its inhibitory effects on EGFR and downstream ERK activation. Conclusions：EGF enhances AQP3 expression and cell migration in cultured mouse melanoma B16 cells. EGFR/ERK activation is involved in this process. These results may provide a new potential therapeutic target in melanoma.

关 键 词：表皮生长因子 水通道蛋白3 黑素瘤细胞 信号通路 小鼠 

分 类 号：R739.5[医药卫生—肿瘤] Q952.5[医药卫生—临床医学]