氯丙嗪对肺腺癌A549细胞恶性生物学行为的抑制作用

Inhibitory Effect of Chlorpromazine on Malignant Biological Behavior of Lung Adenocarcinoma A549 Cells Via CaMKⅡ/c-Fos Pathway

目的探讨氯丙嗪对肺腺癌A549细胞的恶性生物学行为是否具有抑制作用及其机制。方法不同浓度氯丙嗪与肺腺癌A549细胞共孵育后,观察该细胞生长能力、克隆形成能力、迁移和侵袭能力的变化,Western blot检测CaMKⅡ、c-Fos的表达情况。结果与对照组比较,MTT结果显示氯丙嗪能显著抑制肺腺癌A549细胞的增殖生长能力,平板克隆形成实验显示氯丙嗪明显抑制肺腺癌A549细胞的克隆形成,Transwell小室迁移、侵袭实验显示氯丙嗪抑制肺腺癌A549细胞的迁移及侵袭,Western blot显示氯丙嗪明显下调肺癌A549细胞的CaMKⅡ、c-Fos蛋白表达(P均<0.05);上述抑制作用均呈剂量依赖性。结论氯丙嗪对肺腺癌A549细胞的增殖、迁移与侵袭等恶性生物学行为有抑制作用,其机制可能与CaMKⅡ/c-Fos通路下调有关。

Objective To investigate the inhibitory effect of chlorpromazine on the malignant biological behavior of lung adenocarcinoma A549 cells and its mechanisms.Methods After incubation of A549 cells with different concentrations of chlorpromazine,the cell growth ability,clonogenic ability,migration and invasion ability were observed,and the expression of CaMKⅡand c-Fos was detected by Western blot.Results Compared with the control group,chlorpromazine could significantly inhibit the proliferation,clone formation and the migration and invasionof lung adenocarcinoma A549 cells.Western blot results showed that chlorpromazine significantly lowered the expression of CaMKⅡand c-Fos protein in lung adenocarcinoma A549(P<0.05),and the inhibitory effects were dose-dependent.Conclusion Chlorpromazine inhibits the proliferation,migration and invasion of lung adenocarcinoma A549 cells,and its mechanism may be related to the downregulation of CaMKⅡ/c-Fos pathway.