CFTR对肺腺癌细胞Calu-3迁移影响的研究

The migration role of CFTR in Calu-3 cell line of lung adenocarcinoma

采用常规培养肺腺癌细胞Calu-3的方法,利用MTT和CCK-8法确定囊性纤维化跨膜传导调节因子(cystic fibrosis transmembrane conductance regulator,CFTR)的激活剂(Genistein)和抑制剂(CFTRinh-172)的最适浓度,用CFTR激活剂和抑制剂的最佳浓度分别处理Calu-3细胞,然后采用划痕实验观测了培养48h后Calu-3细胞迁移的差异.结果表明:MTT法检测激活剂的最佳浓度为25μmol/L;CCK-8法检测抑制剂的最佳浓度为10μmol/L;划痕实验检测得出25μmol/L激活剂组细胞迁移数量((74.2±5.79)个)与对照组细胞迁移数量((134.1±10.04)个)相比具有显著性差异(P=0.00<0.01);10μmol/L抑制剂组细胞迁移数量((148.3±17.70)个)与对照组细胞迁移数量((134.1±10.04)个)相比无显著性差异(P=0.27>0.05).激活剂通过促进CFTR氯离子通道的开放,抑制了肺腺癌肿瘤细胞Calu-3的迁移.

Calu-3 were cultured by conventional method in this paper,and the optimal concentrations of activator and inhibitor of cystic fibrosis transmembrane conductance regulator were determined by MTT and CCK-8 method,the optimal concentrations of the CFTR activator（Genistein） and inhibitor （CFTRinh-172） were added to the cell,detected the migration of cultured Calu3 cells by scratch test in 48 h. The following results were obtained：The optimal concentrations of activator were 25 μmol/L. The Optimal concentrations of inhibitor were 10μmol/L. The results of scratch tests showed that there was significant difference（P=0.00〈0.01） between the number of cell migration of activator（25 μmol/L） group（74.2±5.79） and the number of cell migration of control group（134.1 ±10.04）. There was no significant difference（P=0.27〉0.05） between the number of cell migration of inhibitor（10 μmol/L） group and the number of cell migration of control group （134. 1 ±10. 04）. Activator （Genistein） inhibited the migration of lung adenocarcinoma cells by making the CFTR chloride ion channels open.