地塞米松诱导急性T淋巴细胞白血病细胞耐药及对miR-15b表达的影响  

Dexamethasone induced resistance in acute T lymphatic leukemia and the impact of miR-15b expression

作　　者：王慧敏[1] 欧阳涓[1] 滕军旗[1] 陈培松[1] 姜傥[1] 

机构地区：[1]中山大学附属第一医院检验科,广东广州510080

出　　处：《热带医学杂志》2016年第6期695-698,共4页Journal of Tropical Medicine

基　　金：国家自然科学基金青年科学基金项目(81101316)

摘　　要：目的建立地塞米松(DEX)诱导急性T淋巴细胞白血病(T-ALL)细胞糖皮质激素获得性抵抗的实验模型,探讨DEX诱导对miR-15b表达的影响。方法用不同浓度DEX、时长作用糖皮质激素敏感T-ALL细胞系CEM/C7,获得耐药细胞系CEM/C7R;采用Annexin V-FITC/PI双染凋亡试剂盒检测细胞凋亡率;同时处理提取CEM/C7、CEM/C7R及耐药细胞系CEM/C1细胞总RNA,利用荧光定量RT-PCR检测三个细胞系miR-15b表达情况。结果 CEM/C7细胞系经10 nmol/L DEX诱导4周可以获得DEX耐药细胞系CEM/C7R;停用DEX诱导后,检测CEM/C7R细胞株凋亡率仅为(5.87±1.21)%,较CEM/C7细胞凋亡率(87.16±2.28)%明显降低,差异有统计学意义(P<0.05);DEX处理后,CEM/C7R细胞中miR-15b表达明显较CEM/C7细胞以及固有耐药细胞系CEM/C1减低,差异有统计学意义(P<0.05)。结论 CEM/C7经长期低剂量DEX处理可获得GC耐药性;miR-15b在DEX耐药细胞系中表达水平减低,提示miR-15b对急性淋巴细胞白血病DEX反应性可能具有调控作用。Objective Toestablish a model of dexamethasone（DEX） induced resistance and the impact of miR-15 b expression in acute T lymphocyte leukemia（T-ALL）. Methods GC sensitive CEM / C7 cells was treated with DEX, and then the apoptosis rate measured by Annexin V-FITC / PI kit was compared with the original cell;the relative expression of miR-15 b was determined by Real-time RT-PCR. Results GC resistance of CEM / C7 R cells could be induced by chronic treatment with 10 nmol / L DEX for 4 weeks, and apoptosis rate was significantly reduced. Mi R-15 b expression was significantly down regulated as compared with CEM / C7 and CEM / C1. Conclusion After long-term treatment of low-dose DEX, CEM / C7 can aquire GC resistance;miR-15 b expression was reduced in DEX resistant cell line indicating that miR-15 b may regulate GC responsiveness in T-ALL.

关 键 词：糖皮质激素 急性T淋巴细胞白血病 miR-15b 

分 类 号：R733.7[医药卫生—肿瘤]