紫草素抑制非小细胞肺癌A549侵袭和迁移能力

目的:肺癌是全球发生率和死亡率最高的癌症。本文旨在探索紫草素对非小细胞肺癌(NSCLC)细胞A549运动能力的影响及其分子机制。方法:CCK-8检测细胞活力。Transwell分析细胞侵袭能力。划痕试验检测细胞迁移能力。蛋白印迹分析血管内皮细胞生长因子(VEGF)、基质金属蛋白酶14(MMP-14)、纤维连接蛋白(FN)、波形蛋白Vimentin、PI3K、pAKT和p53的表达。结果:紫草素可减弱A549细胞活力。与对照组相比,紫草素(20、50、100 mmol/L)组细胞侵袭和迁移能力明显降低(P<0. 05)。紫草素(20、50、100 mmol/L)组VEGF,MMP-14,Fn和Vimentin的表达明显低于对照组(P<0. 05)。与A549组相比,PI3K/AKT通路激活剂IGF-1组PI3K和p-AKT表达升高,p53表达减弱(P <0. 05)。与IGF-1组相比,紫草素(20、50、100 mmol/L)组PI3K和p-AKT表达降低,p53表达升高(P<0. 05)。结论:紫草素可通过PI3K/AKT信号通路抑制NSCLC细胞A549侵袭和迁移能力。

Shikonin suppresses invasion and migration of non-small cell lung cancer cells A549

Objective:Lung cancer is the most commonly diagnosed cancers and the leading cause of cancer death worldwide.This study aims to explore the effect and mechanism of shikonin on invasion and migration of non-small cell lung cancer cells A549.Methods:Cell viability was detected by CCK-8.Transwell assay was performed to analyze the invasion of A549.Wound healing assay was used to measure the migration of A549.The expression of vascular endothelial growth factor(VEGF),matrix metalloprotein 14(MMP-14),fibronectin(FN),Vimentin,PI3K,p-AKT and p53 was tested by Western blot.Results:Cell viability of A549 was reduced by shikonin.Compared with control group,the invasion of A549 in shikonin group(20,50,100 mmol/L)was decreased as well as the migration(P<0.05).The expression of VEGF,MMP-14,Fn and Vimentin in shikonin group(20,50,100 mmol/L)was lower than control group(P<0.05).Compared with A549 group,the expression of PI3K and p-AKT in IGF-1 group was increased with alleviated expression of p53(P<0.05).Compared with IGF-1 group,the expression of PI3K and p-AKT in shikonin group(20,50,100 mmol/L)declined with enhancive expression of p53(P<0.05).Conclusion:Shikonin suppresses invasion and migration of NSCLC cells A549 through inhibition of PI3K/AKT signal pathway.