张凌云;曲秀娟;滕月娥;刘云鹏;侯科佐;

• 1:中国医科大学附属第一医院

摘要：

目的探讨磷脂酰肌醇-3-激酶/丝苏氨酸蛋白激酶(PI3K/Akt)信号通路在核因子-κB受体活化因子配体(RANKL)诱导的乳腺癌细胞迁移中的作用。方法 Transwell法测定RANKL刺激后MDA-MB-231细胞迁移能力的改变。蛋白印迹法检测MDA-MB-231细胞表面RANK蛋白的表达及RANKL刺激后pAkt及Akt的表达;检测数据用x珚±s表示,采用SPSS 16.0软件进行t检验。结果 MDA-MB-231细胞表达RANK蛋白,RANKL诱导MDA-MB-231细胞迁移能力增强,RANKL的圈套受体骨保护素(OPG)可阻断RANKL诱导的细胞迁移(P<0.01)。RANKL刺激后MDA-MB-231细胞p-Akt表达升高,PI3K抑制剂LY294002抑制RANKL诱导的细胞迁移(P<0.01)。结论 PI3K/Akt信号通路参与RANKL诱导的乳腺癌细胞MDA-MB-231迁移。

关键词： 乳腺肿瘤;细胞运动;核因子-κB受体活化因子配体

Abstract: Objective To evaluate the role of PI3K/Akt in RANKL induced MDA-MB-231 breast cancer cells migration.Methods Transwell assayed the migration of human breast cancer cell lines MDA-MB-231 after stimulated by RANKL specific inhibitors.Western blotting assayed the expression of phospho-Akt,Akt,and RANK.The significance of the difference between the groups was assessed by the Student's two-tailed t-test,and P<0.05 was considered significant in all statistical analyses.Results Western blotting showed that RANK was expressed in human breast cancer cell line MDA-MB-231 and RANKL increased the migration of breast cancer cells significantly.The decoy receptor of RANKL,rPG(recombinant osteoprotegerin),significantly blocked RANKL-induced breast cancer cells migration(P<0.01).The expression of p-Akt increased at 30 minutes after RANKL stimulating.LY294002,the PI3K/Akt inhibitor,significantly inhibited RANKL-induced breast cancer cells migration(P<0.01).Conclusion PI3K/Akt was involved in RANKL-induced breast cancer cells MDA-MB-231 migration.

Keywords: Breast neoplasms;Cell movement;RANKL

基金项目: 国家青年科学基金(30700807);; 辽宁省教育厅科技项目(2010225032)

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