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三氧化二砷诱导慢性髓系白血病细胞G_2/M周期停滞及其机理 被引量:4

Mechanism of G_2/M Cycle Arrest Induced by Arsenic Trioxide in Chronic Myelogenous Leukemia Cells
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摘要 目的 研究三氧化二砷对慢性髓系白血病细胞的体外作用特点及其机理。方法 将三氧化二砷与慢性髓性白血病细胞系K562作用后 ,测定细胞的生长曲线及活性 ,流式细胞测量术检测细胞凋亡和细胞周期分布的改变 ;同时 ,采用RT PCR方法检测药物作用前后细胞周期相关基因表达的变化。结果 ①三氧化二砷明显抑制K562细胞的生长 ,其作用呈时间和浓度依赖性 ;②三氧化二砷诱导K562细胞凋亡的作用较弱 ,但可明显诱导K562细胞在G2 /M期停滞 ,此效应也呈时间和浓度依赖性 ;③三氧化二砷作用后 ,细胞周期抑制基因p57表达明显上调 ,而细胞周期促进基因cyclinB的表达受到抑制。结论 三氧化二砷能有效抑制慢性髓系白血病细胞的生长 ,其机理主要为诱导细胞G2 /M期周期停滞 ; Objective To investigate the effects and it s possible mechanisms of arsenic trioxide (As 2O 3) on chronic myelogenous leuke mic (CML) cells in vitro. Methods After CML cell line K562 was incubated with As 2O 3, the growth curve and activity of the cells were measured. The apoptosis and the changes in cell cycle were detected by using flow cytometry. The expression of cell cycle related genes before and after administration of As 2O 3 was detect ed by RT-PCR. Results As 2O 3 could inhibit the growth of K562 cells in a t ime- and dose-dependent manner. As 2O 3 could weakly induce the apoptosis of K562 cells, but could significantly induce G 2/M arrest of K562 cells in a tim e- and dose-dependent manner. As 2O 3 could up-regulate the expression of p 57, but inhibit the expression of cyclinB gene. Conclusion As 2O 3 can effectively inhibit the growth of CML cells by inducing G 2/M arrest, which is related with the change in the express ion of cell cycle related genes.
出处 《华中科技大学学报(医学版)》 CAS CSCD 北大核心 2003年第6期610-612,615,共4页 Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金 日中医学协会世川医学奖学金特别研究员项目 (2 0 0 1)资助
关键词 三氧化二砷 诱导 慢性髓系白血病 细胞周期 p57基因 arsenic trioxide chronic myelogenous leukemia cel l cycle p57 gene
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