毛蕊异黄酮通过RAS/RAF/MEK/ERK信号通路抑制肺癌细胞增殖和迁移的作用机制

Proliferation and Migration of Lung Cancer Cells Inhibited by Calycosin through RAS/RAF/MEK/ERK Signaling Pathway

目的探讨毛蕊异黄酮(Calycosin)通过RAS/RAF/MEK/ERK信号通路抑制肺癌细胞增殖、迁移的作用机制。方法将肺癌A549细胞分为空白对照组和毛蕊异黄酮20、40、80μmol/L 3个浓度组。MTT法检测细胞存活率;Western Blot检测肺癌A549细胞RAS、p-RAF、p-MEK和p-ERK蛋白的表达;细胞集落试验和划痕试验观察肺癌A549细胞的增殖和迁移。结果当毛蕊异黄酮浓度在80μmol/L以下时,毛蕊异黄酮无明显细胞毒性。毛蕊异黄酮可抑制RAS、p-RAF、p-MEK和p-ERK蛋白表达,且抑制效果呈剂量依赖性;毛蕊异黄酮对肺癌A549细胞增殖和迁移的抑制作用呈剂量依赖性。结论毛蕊异黄酮能够通过RAS/RAF/MEK/ERK信号通路抑制肺癌A549细胞增殖和迁移。

Objective To investigate the effect of Calycosin on the proliferation and migration of lung cancer cells and its related mechanism.Method Lung cancer cell A549 were divided into four groups:control group and three Calycosin groups(20μmol/L,40μmol/L and 80μmol/L).Cell survival rate was detected by MTT assay.The expressions of RAS,p-RAF,p-MEK and p-ERK proteins in A549 cells were detected by Western Blot.The proliferation and migration of A549 cells were observed by cell colony assay and scratch assay.Results Calycosin had no obvious cytotoxicity at concentrations below 80μmol/L.Calycosin could dose-dependently inhibit the expression of RAS,p-RAF,p-MEK and p-ERK proteins;Calycosin could dose-dependently inhibit the prolifer-ation and migration of A549 cells.Conclusion Calycosin inhibits the proliferation and migration of lung cancer cell A549 through RAS/RAF/MEK/ERK signaling pathway.