PI3K/Akt信号通路在RANKL诱导的MCF-7乳腺癌细胞迁移中的作用

PI3K/AKT was involved in RANKL-induced breast cancer cell MCF-7 migration

目的:核因子-κB受体活化因子配体(RANKL)能促进表达RANK的上皮癌细胞迁移至骨,与乳腺癌骨转移密切相关。本文探讨磷脂酰肌醇-3-激酶/丝苏氨酸蛋白激酶(phosphoinositide3-kinase/serine/threonine protein kinase PI3K/Akt)信号通路在RANKL诱导的乳腺癌MCF-7细胞迁移中的作用。方法:流式细胞仪检测MCF-7细胞表面RANK蛋白的表达;Transwell法测定RANKL刺激后MCF-7细胞迁移能力的改变;Western-blot检测MCF-7细胞RANKL刺激后p-Akt及Akt的表达。SPSS 16.0软件分析实验数据。结果:MCF-7细胞表达RANK蛋白,RANKL诱导MCF-7细胞迁移能力显著增强,RANKL的圈套受体OPG可阻断RANKL诱导的细胞迁移。RANKL刺激后MCF-7细胞p-Akt表达在1、5分钟时一过性升高,PI3K抑制剂LY294002显著抑制RANKL诱导的细胞迁移。结论:PI3K/Akt信号通路参与RANKL诱导的乳腺癌细胞系MCF-7迁移。

Objective：Receptor activator for nuclear factor kappa B ligand / receptor activator for nuclear factor kappa B（RANKL/RANK）pathway is critical for RANK-expressing cancer cells to home to bones.There is few report about the role of phosphoinositide 3-kinase/serine/threonine protein kinase（PI3K/Akt）pathway in regulation of cancer cells migration by RANKL.The present study aimed to evaluate the role of PI3K/Akt in RANKL-induced breast cancer MCF-7 cells migration.Methods： Flow cytomety was used to detect the surface RANK expression in human breast cancer cell lines MCF-7.Transwell was used to test the migration of MCF-7,Western blotting test the expression of phospho-Akt and Akt.Results： RANK was expressed in human breast cancer cell line MCF-7,and RANKL increased the migration of breast cancer cells significantly.The decoy receptor of RANKL,OPG,blocked RANKL-induced breast cancer cells migration.The Expression of p-Akt increased from 1 to 5 minutes after RANKL stimulating,LY294002,PI3K/Akt inhibitor significantly inhibited RANKL-induced breast cancer cells migration.Conclusion： PI3K/Akt was involved in RANKL-induced breast cancer MCF-7 cells migration.