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目的 :探讨 TPA诱发人喉鳞癌细胞凋亡的规律及基因调控机制。方法 :应用电镜及流式细胞仪分析技术进行观察和检测。结果 :1nmol/L TPA作用 12小时 ,可明显地诱发 Hep- 2细胞凋亡 (凋亡率为 11.18% ) ,2 4小时内 ,其诱导效率呈时间、剂量依赖性增强 ,最大凋亡率为 2 7.8% (10 0 nmol/L TPA诱发 2 4小时 )。细胞分裂阻滞于 G1期。 Bcl- 2的表达在 12小时出现明显的抑制 ,而 Fas在 6小时即出现较高的表达。 4 8小时内 ,两种基因的表达呈现出明显的负相关 (r=- 0 .92 80 ,P <0 .0 1)。结论 :TPA能够诱发人喉鳞癌细胞凋亡 ,Bcl- 2和 Fas在 TPA诱发的人喉鳞癌细胞凋亡过程中可能起着重要的作用
Objective: To investigate the regularity and gene regulatory mechanism of TPA-induced human laryngeal squamous cell carcinoma cell apoptosis. Methods: Electron microscopy and flow cytometry analysis were used to observe and test. Results: The apoptosis of Hep-2 cells was induced by 1 nmol / L TPA for 12 hours (the apoptosis rate was 11.18%). Within 24 hours, the induction efficiency was increased in a time-and dose-dependent manner. The maximum apoptosis rate was 2 7.8% (10 0 nmol / L TPA induced 24 hours). Cell division arrests in G1 phase. The expression of Bcl-2 was significantly inhibited at 12 hours, while Fas increased at 6 hours. Within 8 hours, the expression of the two genes showed a significant negative correlation (r = - 0.9280, P <0.01). Conclusion: TPA can induce the apoptosis of human laryngeal squamous cell carcinoma. Bcl-2 and Fas may play important roles in TPA-induced apoptosis of human laryngeal squamous cell carcinoma