摘要
目的 探讨has-miR-203与慢性粒细胞白血病三氧化二砷(As2O3)治疗的敏感性的关系及可能的作用机制.方法 体外培养K562细胞,利用LipofectamineTM 2000将miR-203模拟物转染至K562细胞,流式细胞术检测转染效率,MTT法检测使用miR-203,As2O3以及两者联合使用对细胞增殖的抑制率,并计算IC50;最后用金正均Q值法评价用药效果.结果 miR-203转染至K562细胞,联合As2O3显著抑制K562细胞增殖,抑制效果较各单独使用组作用明显增强.As2O3浓度为0.05,0.1,0.2和0.4 μmol/L时的抑制率分别为24.0%±5.0%,33.1%±1.5%,39.4%±3.4%和47.1%±5.5%.micRNA-203浓度为5,10,20和40 μmol/L时的抑制率分别为27.0%±6.7%,38.8%±3.2%,44.6%±3.0%和59.6%±3.7%.不同浓度梯度的As2O3联合20 μmol/L的micRNA-203抑制率分别为46.9%±3.2%,48.9%±3.9%,50.2%±5.5%和56.1%±1.9%.结论 当一定浓度的miR-203与不同浓度梯度的As2O3联合之后,对K562细胞的增殖抑制表现为相加作用,提高了K562细胞对As2O3的敏感性,为白血病的治疗提供新的依据.
Objective To study the effect of hsa-miR-203 for enhancing the arsenic trioxide sensitivity of leukemic K562 cells and its possible acting mechanism. Methods Cultured K562 cells in vitro,and hsa-miR-203 minies was transfected to K562 cells using LipofectamineTM 2000. The transfeeted rates were determined by flow cytometry. The inhibitory effects of ATO and miR-203 ,used singly or in combining on cell proliferation were detected by MTT. Their inhibition rate and IC^0 were cal- culated. Evaluate the drug effects with jinzhengjun Q valus. Results The growth inhibition rates was obivously enhanced when arsenic trioxidecombining with miR-203. Arsenic trioxide using singly, the inhibition rate were 24.0 %± 5.0 %, 33.1% ±1.5% ,39. 4%±3.4% and 47.1% ±5.5% ,respectively. MiR-203 using singly,the inhibition rate were 27.0% -t-6. 7%, 38. 8%±3.2% ,44. 6%±3. 0% and 59. 6%±3.7% ,respectively. The inhibition rate were 46.9%±3.2% ,48. 9% ±3.9%, 50. 2 % ± 5.5 % and 56.1%±1.9 %, respectively. When the same concentrations of miR-203 combined with arsenic trioxide. Conclusion Combined use of miR-203 and arsenic trioxide,could increase the sensitivity of K562 cells to As2O3 ,which provides a novel potential approach for treatment of leukemia.
出处
《现代检验医学杂志》
CAS
2013年第3期106-109,共4页
Journal of Modern Laboratory Medicine
基金
广东省科技厅社会发展项目(20118080702011).