RANKL通过激活Akt及ERK介导胃癌细胞迁移  

RANKL Induces Gastric Cancer Cells Migration by Activation of Akt and ERK Signaling Pathways

作　　者：王妍[1] 刘云鹏[1] 曲秀娟[1] 徐玲[1] 张凌云[1] 李智[1] 侯科佐[1] 汪茜[2] 刘静[1] 

机构地区：[1]中国医科大学附属第一医院肿瘤内科,沈阳110001 [2]中国医科大学附属第四医院肿瘤内科,沈阳110032

出　　处：《中国医科大学学报》2013年第7期591-594,共4页Journal of China Medical University

基　　金：国家自然科学基金(81172198;81201802);辽宁省高等学校杰出青年学者成长计划(LJQ2011082)

摘　　要：目的探讨核因子受体活化因子(RANK)及其配体RANKL能否诱导胃癌细胞迁移及其作用机制。方法采用流式细胞学技术检测BGC823胃癌细胞中RANK的表达;采用Transwell检测细胞迁移能力;采用Western blot检测细胞信号的变化情况。结果流式细胞检测结果显示:BGC823胃癌细胞中有RANK表达。Transwell及Western blot检测结果显示RANKL能够通过活化Akt和ERK诱导BGC823细胞迁移。RANKL诱导的胃癌细胞迁移可被骨保护素、PI3K抑制剂LY294002以及MEK抑制剂PD98059逆转。结论 RANKL可通过激活PI3K及MEK通路诱导胃癌细胞迁移。Objective To investigate whether RANKL/RANK pathway can induce gastric cancer cells migration. Methods The expres- sion of RANK was detected by flow eytometry. Cell migration was tested by Transwell assay. Changes of signaling pathways were investigated using Western blot analysis. Results The results showed that RANK was expressed in BGC823 gastric cancer cells and RANKL could induce BGC823 cells migration by activating Akt and ERK signaling pathways. The effect of RANKL can be reversed by osteoprotegerin, PI3K inhibitor LY294002 and MEK inhibitor PD98058. Condusion RANKL was proved to induce the migration of gastric cancer cells at least partially through the activation of PI3K and MEK signaling pathways.

关 键 词：核因子受体活化因子 核因子受体活化因子配体 胃癌细胞 迁移 

分 类 号：R73[医药卫生—肿瘤]