Objective: To study the effect of MLN4924 on the proliferation and apoptosis of lung epithelial carcinoma A549 cells. Methods: A549 cells were treated with MLN4924 at different concentrations and incubation times. The inhibition rate of cell growth was detected using the cell counting kit-8 (CCK-8) assay. Apoptosis was observed using Hoechst 33342 and flow cytometry. The protein expression of the associated proteins in cell apoptosis, including caspase-3, NF-KB p65, and CDT1, was determined through Western blot analysis. Results: The proliferation of A549 cells decreased when the concentration of MLN4924 increased or the incubation time was prolonged. MLN4924 induced S phase cell cycle arrest. The protein expression of the associated proteins caspase-3 and CDT1 was higher than that of the control group. NF-KB p65 was lower than that in the control group. Conclusion: MLN4924 effectively inhibited the proliferation and induced cell apoptosis in A549 cells. MLN4924 treatment induced the S phase cell cycle arrest, increased the caspase-3 protein expression, and inhibited the NF-KB pathway activation.%目的:观察MLN4924对人肺腺癌A549细胞增殖、凋亡的影响,探讨MLN4924促进凋亡的作用机制.方法:不同浓度的MLN4924作用细胞不同时间后,采用CCK-8检测细胞增殖抑制率；Hoeehst33342荧光染色、流式细胞仪检测细胞凋亡率及细胞周期；Western blot检测凋亡相关蛋白Caspase-3、NF-κB p65及CDT1相对表达量.结果:MLN4924能够明显抑制A549细胞的增殖,并且具有浓度和时间依赖性.流式细胞仪检测结果显示药物作用后,细胞被阻滞在S期.Western blot结果显示药物作用后细胞内Caspase-3、CDT1蛋白的表达量增加,而NF-κB p65的表达量减少.结论:MLN4924能够明显抑制A549细胞增殖、促进细胞凋亡,其相关机制为MLN4924可阻滞细胞于S期,增加Caspase-3蛋白表达,抑制NF-κB通路的激活.
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