表皮生长因子受体/丝氨酸/苏氨酸蛋白激酶通路对小鼠黑素瘤B16细胞迁移的影响  

Migration of B16 mouse melanoma cells induced by epidermal growth factor through EGFR/AKT pathways

作　　者：严军华[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》2011年第8期464-466,共3页Journal of Clinical Dermatology

摘　　要：目的:研究表皮生长因子受体(EGFR)/丝氨酸/苏氨酸蛋白激酶(AKT)通路对小鼠黑素瘤B16细胞迁移的影响。方法:蛋白质免疫印迹方法分析各蛋白的表达;phagokinetic track motility法观察细胞的迁移。结果:表皮生长因子(EGF)能促进小鼠黑素瘤B16细胞迁移;AKT抑制剂(wortmannin)和水通道蛋白-3(aquaporins-3,AQP3)抑制剂(CuSO_4)能抑制小鼠黑素瘤B16细胞迁移;EGF可诱导AKT磷酸化,EGF处理后5 min磷酸化AKT达到高峰。wortmannin和CuSO_4可抑制细胞中AQP3的表达。结论:在小鼠黑素瘤B16细胞中,EGF通过磷酸化EGFR,激活AKT,进而使AQP3表达上调,促进B16细胞迁移。这一通路可被AKT和AQP3抑制剂阻断,这些涉及的信号通路可能成为潜在的治疗黑素瘤的靶点。Objective： To investigate the effect of EGFR/AKT pathways on the migration of B16 cells （mouse melanoma cell line）. Methods： Cultured B16 cells were treated with EGF and/or various reagents and subjected to cell migration assay by phagokinetic track motility. The expression or activation of proteins was analyzed by SDS-PAGE and Western blotting. Results： EGF promoted the migration of cultured B16 mouse melanoma cells, the cell migration was inhibited by AKT in- hibitor（wortmannin） and AQP3 water transport inhibitor （CuSO4）. EGF induced the phosphorylation of AKT. The AKT inhibitor （wortmannin） and the AQP3 inhibitor（CuSO4）suppressed the activation of AQP3. Conclusions： The phosphorylation of EGFR induced by EGF, subsequently AKT activation and upregulated AQP3 expression are involved in the migration of B16 cells, which could be blocked by wortmannin or CuSO4 respectively. These results indicate that EGFR/AKT pathway might be a new potential therapeutic target in the treatment of melanoma.

关 键 词：表皮生长因子 水通道蛋白3 黑素瘤细胞 丝氨酸/苏氨酸蛋白激酶 

分 类 号：R739.5[医药卫生—肿瘤]