|
|||||
|
|
| 三氧化二砷诱导慢性髓系白血病细胞G2/M周期停滞及其机理 | |
| 引用本文： | 陈智超,大西一功,游泳,罗建明,邹萍,大野龙三.三氧化二砷诱导慢性髓系白血病细胞G2/M周期停滞及其机理[J].华中科技大学学报(医学版),2003,32(6):610-612,615. |
| 作者姓名： | 陈智超 大西一功 游泳 罗建明 邹萍 大野龙三 |
| 作者单位： | 1. 华中科技大学同济医学院血液病研究所,武汉,430022 2. 日本滨松医科大学第三内科,滨松,431-3192 3. 日本爱知县癌中心医院,名古屋,464-8681 |
| 基金项目： | 日中医学协会世川医学奖学金特别研究员项目(2001)资助 |
| 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；该效应与细胞周期相关基因的表达变化有关。 |
| 关 键 词： | 三氧化二砷 诱导 慢性髓系白血病 细胞周期 p57基因 |
Mechanism of G2/M Cycle Arrest Induced by Arsenic Trioxide in Chronic Myelogenous Leukemia Cells |
|
| Chen Zhichao ,Ohnishi Kazunori ,You Yong et al Institute of Hematology,Tongji Medical College,Huazhong University of Scie nce and Technology,Wuhan Third.Mechanism of G2/M Cycle Arrest Induced by Arsenic Trioxide in Chronic Myelogenous Leukemia Cells[J].Journal of Huazhong University of Science and Technology(Health Sciences),2003,32(6):610-612,615. | |
| Authors: | Chen Zhichao Ohnishi Kazunori You Yong Institute of Hematology Tongji Medical College Huazhong University of Scie nce and Technology Wuhan Third |
| Institution: | Chen Zhichao 1,Ohnishi Kazunori 2,You Yong 1 et al 1 Institute of Hematology,Tongji Medical College,Huazhong University of Scie nce and Technology,Wuhan 430022 2 Third Department of Medicine,Hamamatsu Medical University,Hamamatsu,Japan 431-3192 |
| Abstract: | 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. |
| Keywords: | arsenic trioxide chronic myelogenous leukemia cel l cycle p57 gene |
| 本文献已被 CNKI 维普 万方数据 等数据库收录！ | |