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目的:观察西妥昔单抗诱导人喉鳞状细胞癌细胞株Hep-2凋亡的敏感性,并探讨西妥昔单抗与顺铂、放射线联合应用对Hep-2细胞的杀伤效应及机制。方法:采用CCK-8试剂盒分别检测西妥昔单抗、顺铂、放射线对Hep-2生长抑制率,流式细胞仪检测不同干预方案对Hep-2凋亡率及细胞周期分布情况。结果:不同浓度西妥昔单抗对Hep-2细胞均有抑制作用,并在一定浓度范围内呈时间-剂量依赖性,24h半数抑制浓度为1 036.84μg/ml;顺铂,放射线分别与西妥昔单抗联合应用时,Hep-2凋亡率显著高于顺铂、放射线单独或联合应用(P<0.01),并产生G0/G1期阻滞。结论:Hep-2细胞对西妥昔单抗诱导的细胞凋亡敏感,顺铂和(或)放射线与西妥昔单抗联用对Hep-2细胞的增殖具有协同抑制效应;显著的凋亡诱导作用和对Hep-2细胞周期的影响为其机制之一,为临床喉鳞状细胞癌靶向EGFR并联合放化疗方案提供了理论依据。
Objective: To observe the sensitivity of cetuximab to induce apoptosis of human laryngeal squamous cell carcinoma cell line Hep-2 and to investigate the killing effect and mechanism of cetuximab in combination with cisplatin and radiation on Hep-2 cells . Methods: The inhibitory rates of cetuximab, cisplatin and radiation on the growth of Hep-2 cells were detected by CCK-8 kit. The apoptosis rate and cell cycle distribution of Hep-2 cells were detected by flow cytometry. Results: Cetuximab could inhibit the proliferation of Hep-2 cells in a dose-and time-dependent manner. The half inhibitory concentration was 1036.84μg / ml at 24h. The apoptosis rate of Hep-2 was significantly higher than that of cisplatin and radiotherapy alone or in combination (P <0.01). CONCLUSION: Hep-2 cells are sensitive to cetuximab-induced apoptosis. Synergistic inhibitory effect of cisplatin and / or radiation with cetuximab on the proliferation of Hep-2 cells was observed. Significant apoptosis Inducing effect and the effect on the cell cycle of Hep-2 cells are one of its mechanisms, which provides a theoretical basis for clinical targeting of EGFR combined with chemoradiotherapy in laryngeal squamous cell carcinoma.