CyclinL2在化疗药物诱导肺癌细胞凋亡中的作用

目的:探讨cyclinL2基因在化疗药物顺铂(DDP)、长春瑞滨(NVB)和多西紫杉醇(DOC)诱导的肺癌细胞凋亡中的作用。方法:用肺腺癌A549细胞株进行培养传代,MTT试验检测DDP、NVB和DOC不同药物浓度对肺癌细胞生长的抑制作用,以及CyclinL2转染后对该细胞生长的抑制作用的影响。同时利用流式细胞术定量检测细胞凋亡。结果:不同浓度DDP、NVB和DOC对肺癌细胞生长均有明显的抑制作用,并有浓度的依赖性。细胞凋亡率和CyclinL2基因表达率成正相关。结论:CyclinL2基因在化疗药物诱导肺癌细胞凋亡中起重要作用。

The Role of CyclinL2 in Chemotherapy-induced Apoptosis of A549 Lung Cancer Cells

Objective: To investigate the effects of cyclinL2 on apoptosis in human lung cancer cells treated with cisplatin (DDP), vinorelbine (NVB) and docetaxel (DOC). Methods: The lung adenocarcinoma cell line A549 was chosen for this experiment. The inhibitory action of chemotherapeutic drugs on A549 cells was assayed using the MTT test. Plasmid pCCNL2-wt containing a full-length coding region of the human cyclinL2 was employed for the transfection. Parental cells and cells transfected with empty vector were used as the controls. Apoptosis was assayed by flow cytometry. Results: All three drugs obviously inhibited growth of the lung cancer cells in a dose-dependent manner. The apoptosis and inhibition ratios were higher in the cells overexpressing the cyclinL2 gene than in the control groups. Conclusion: The cyclinL2 gene may play a critical role in lung cancer cell apoptosis induced by chemotherapeutic drugs.