胰岛素对前列腺癌LNCaP细胞的抑制作用  

Inhibitory effect of insulin on prostate cancer LNCaP cell line

作　　者：王琛[1] 唐悦清[1] 闫磊[1] 焦伟[1] 周尊林[1] 徐忠华[1] 

机构地区：[1]山东大学齐鲁医院泌尿外科,山东济南250012

出　　处：《山东大学学报（医学版）》2014年第7期22-27,共6页Journal of Shandong University:Health Sciences

基　　金：山东省科学技术发展项目(26010104011178)

摘　　要：目的观察胰岛素对前列腺癌LNCaP细胞系增殖、活力、迁移与侵袭能力的影响,并探讨其机制。方法胰岛素刺激LNCaP细胞后,采用实时荧光定量聚合酶链反应(Real-time PCR)、蛋白免疫印迹(Western blotting)、免疫细胞化学(ICC)法检测胰岛素受体表达变化;细胞计数法、四唑盐法(MTT)、细胞划痕、细胞侵袭实验(Transwell)检测细胞增殖、活力、迁移和侵袭能力;Western blotting检测Ras、ERK1/2、MEK1/2蛋白水平表达变化。结果胰岛素可促进LNCaP细胞胰岛素受体的表达,抑制其增殖、活力、迁移及侵袭能力,同时抑制其Ras的表达及ERK1/2、MEK1/2的磷酸化(P<0.05)。结论胰岛素可通过胰岛素受体抑制Ras-MEK-ERK信号通路的活化,从而抑制LNCaP细胞的增殖、活力、迁移及侵袭。Objective To study the inhibitory effect of insulin on LNCaP human prostate cancer cell line and its possible mechanism. Methods After LNCaP cells were treated with insulin,the expression of insulin receptor was detected with Real-time PCR,immunocytochemistry and Western blotting. The effects of insulin on cell growth,viability,migration and invasion were measured by cell counting,MTT,wound healing and Transwell. The activation of MAPK pathway was determined by Western blotting. Results Insulin increased the mRNA and protein expressions of INSR in LNCaP cells,and inhibited the cell growth,viability,migration and invasion. Expressions of key proteins in the MAPK pathway,including Ras,p-MEK and p-ERK,were significantly lowered by insulin. Conclusion Insulin can inhibit prostate cancer LNCaP cell line through MAPK signal pathway.

关 键 词：前列腺肿瘤 胰岛素 胰岛素受体 MAPK信号通路 

分 类 号：R737.25[医药卫生—肿瘤]