摘要
目的探讨三氧化二砷(As2O3)对食管癌离体肿瘤细胞EC-1的放射增敏作用,并探讨其机制。方法利用多靶单击数学模型拟合放射剂量-细胞存活曲线,观察As2O3对食管癌细胞株EC-1的放射增敏作用。流式细胞法观察As2O3对细胞周期分布及细胞凋亡的影响。结果 As2O3对食管癌细胞株EC-1有明显的放射增敏效应,3μmol/L As2O3作用48 h的放射增敏比为1.285。药物作用后G2/M期细胞比例增加,G0/G1期和S期细胞比例减少;细胞凋亡指数增加,与对照组相比,差异有统计学意义(P<0.05)。结论 As2O3对食管癌细胞株EC-1有明显的放射增敏效应。放射增敏的机制可能与As2O3抑制EC-1细胞的修复能力、使细胞周期阻滞在G2/M期、G0/G1期和S期细胞减少以及凋亡增加有关。
Objective To explore the radiosensitivity effect and mechanism of action of Arsenic trioxide（Arsenic trioxide,As2O3） on esophageal carcinoma EC-1 cell line.Method The radiosensitivity effect of Arsenic trioxide（As2O3） on esophageal carcinoma EC-1 cell line by fitting the irradiation dose-survival curve using ＇multitarget click mathematical model＇.Flow cytometry（FCM） was used to detect the changes of cell apoptosis and cell cycle.Results As2O3 had an obvious radiosensitivity effect on esophageal carcinoma EC-1 cells.After treatment with 3 μmol/L As2O3 for 48 hours,the sensitization enhancement ratio（SER） is 1.285.The G2/M phase ratio is increased while the G0/G1 phase and the S phase ratio decreased after treatment.The apoptotic index was significantly increased（P0.05）,compared with the control group.Conclusion As2O3 has an obvious radiosensitivity effect on esophageal carcinoma EC-1 cells,and the mechanism of action may be related to decreased repair capacity of the EC-1 cells,the cell cycle arresting is G2/M phase,the decreased cell number of G0,G1 and S phase and increased apoptosis.
出处
《肿瘤防治研究》
CAS
CSCD
北大核心
2012年第6期667-670,共4页
Cancer Research on Prevention and Treatment
基金
河南省科技厅基金资助项目(082300450160)
