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目的 研究肿瘤坏死因子 (TNFα)和足叶乙甙 (VP16 )联合对肺癌细胞包株的作用及其机制。方法 用MTT法检测不同浓度的TNFα、VP16及TNFα联合VP16对人肺癌细胞系A5 4 9的细胞毒作用以及用间接荧光标记法、流式细胞仪观察TNFα、VP16及TNFα联合VP16对A5 4 9的细胞周期、粘附分子表达的影响。结果 TNFα、VP16对A5 4 9细胞的生长抑制作用有剂量依赖关系 ,而TNFα联合VP16对A5 4 9抑制作用较TNFα、VP16作用显著 (P <0 .0 1)。TNFα、TNFα联合VP16能上调CD5 4表达 ,与VP16均能上调CD95表达 ,而粘附分子CD11α、CD18、CD4 0、CD80、CD137等用药后仍不表达。对细胞周期用药后G2 期明显下降 (13.2 %下降至 3.0 % ) ,S期上升 (2 7.3%上升至 4 2 .5 % )。结论 TNFα联合VP16增加A5 4 9的抑制率 ,增强CD5 4、CD95表达。推测TNFα联合VP16对A5 4 9细胞的作用是通过抑制DNA合成及有丝分裂 ,使G0 +G1+S期不能及时转至G2 、M期并促进肺癌细胞凋亡
Objective To investigate the effect of tumor necrosis factor (TNFα) and etoposide (VP16) on lung cancer cell line and its mechanism. METHODS: The cytotoxicity of TNFα, VP16 and TNFα combined with VP16 on human lung cancer cell line A549 was examined by MTT assay, and TNFα, VP16 and TNFα were detected by indirect fluorescent labeling and flow cytometry. The effects of cell cycle and adhesion molecule expression. Results The inhibitory effect of TNFα and VP16 on the growth of A549 cells was dose-dependent, but the inhibitory effect of TNFα combined with VP16 on TNFα and VP16 was significant (P < 0.01). TNFα, TNFα combined with VP16 could up-regulate the expression of CD5, and VP16 could up-regulate the expression of CD95, while adhesion molecules such as CD11α, CD18, CD40, CD80, and CD137 were still not expressed. After the cell cycle, the G2 phase significantly decreased (13.2% to 3.0%), and the S phase increased (27.3% to 42.5%). Conclusion TNFα combined with VP16 increased the inhibition rate of A549 and enhanced CD5 4 and CD95 expression. It is speculated that the effect of TNFα combined with VP16 on A549 cells is through inhibiting DNA synthesis and mitosis, so that G0 + G1 + S phase cannot be timely transferred to G2, M phase and promotes apoptosis of lung cancer cells.