右美托咪定通过调控miR-1307表达对肺癌A549细胞生物学行为的影响

Effect of dexmedetomidine on biological behavior of A549 cells through miR-1307 expession

目的通过检测miR-1307表达水平,分析右美托咪定(dexmedetomidine,Dex)对肺癌A549细胞生物学行为影响的可能机制。方法人肺癌A549细胞接种后培养24h,采用数字表法随机分为4组:肺癌A549细胞组、Dex20μg/ml组、Dex 40μg/ml组及Dex 80μg/ml组;每组每孔设6个平行样,各组细胞培养结束后,通过CCK-8法测定细胞增殖能力,应用Annexin V-FITC/PI双染法观察细胞凋亡,Matrigel膜及Transwell法测定细胞侵袭力及迁移水平,采用实时荧光定量PCR检测各组细胞中miR-1307的表达水平。结果Dex能抑制肺癌A549细胞活力,且作用呈浓度依赖性及时间依赖性;Dex可诱导肺癌A549细胞凋亡,当Dex浓度达到80μg/ml,其凋亡率可升至22.23%;Dex可抑制肺癌A549细胞的迁移与侵袭能力,且呈浓度依赖性。此外,与对照组比较,Dex处理后A549细胞中miR-1307的相对表达量明显下降,且随着Dex浓度的增加下降更为明显。结论Dex能有效抑制肺癌A549细胞的增殖、侵袭、迁移,促进其凋亡,并呈剂量依赖性,其作用可能与其调控miR-1307的表达有关。

Objective To analyze the effect of dexmedetomidine(Dex)on biological behavior of A549 cells through expression of miR-1307.Methods Human lung cancer A549 cells were randomly divided into four groups after being cultured for 24 hours:Lung cancer A549 cell group,Dex 20μg/ml group,Dex 40μg/ml group and Dex 80μg/ml group;Each group has 6 parallel samples per hole.After each group of cell culture,we detected the cell proliferation by CCK-8 method,cell apoptosis by flow cytometry,mir-1307 expression by qRT-PCR,cell invasion and cell migration(Transwell)respectively Results Dex inhibits the viability of lung cancer A549 cells in a concentration-and time-dependent manner.Dex can promote the apoptosis of lung cancer A549 cells,and the apoptosis rate can be increased to 22.23% when the concentration of Dex reaches 80μg/ml,the apoptosis rate can rise to 22.23%.Dex inhibits the migration and invasion of lung cancer A549 cells in a concentration-dependent manner.In addition,the relative expression of miR-1307 in A549 cells after Dex treatment decreased significantly comparing to the control group,and the decline was more noteworthy with the increase of Dex concentration.Conclusion Dex can effectively inhibit the proliferation,invasion,metastasis,and apoptosis of humen A549 cells in a dose-dependent manner,and its efficacy may be related to its regulation of miR-1307 expression.