TAT-N24穿膜融合多肽对白血病细胞系HL60分化的影响  

Effect of cell-permeable fusion peptide TAT-N24 on differentiation of leukemia cell line HL60

在线阅读下载全文

作  者:杨熹[1] 王桂华[1] 曹小年[1] 李国东[1] 傅寅佳[1] 胡俊波[1] 邓豫[2] 

机构地区:[1]华中科技大学同济医学院附属同济医院肿瘤研究所/胃肠外科,武汉市430030 [2]华中科技大学同济医学院附属同济医院肿瘤研究所/普胸外科,武汉市430030

出  处:《实用医学杂志》2013年第13期2078-2080,共3页The Journal of Practical Medicine

基  金:国家973计划项目(编号:2009CB521802);国家自然科学基金资助项目(编号:30872472;30973496;30800569);湖北省自然科学基金资助项目(编号:2008CDB174;2009CDB239)

摘  要:目的:观察TAT-N24穿膜融合多肽对急性髓系白血病细胞株HL60分化的影响。方法:TAT-N24作用于HL60细胞后,采用流式细胞术检测白血病分化指标CD11b及CD14,并观察HL60细胞经TAT-N24处理后的形态学变化,及BrdU/PI双掺入法测定DNA的合成。结果:HL60细胞在TAT-N24处理后,CD11b和CD14表达增高,且增高的趋势呈现TAT-N24浓度依赖性,同时形态学观察呈分化趋势,而且TAT-N24可以协同全反式维甲酸,增强其促进分化的作用。与此同时,BrdU/PI双掺入法显示TAT-N24使HL60细胞的增殖发生抑制。结论:TAT-N24穿膜融合多肽可促进急性髓系白血病细胞株HL60的分化,抑制其增殖,联合应用TAT-N24和全反式维甲酸具有明显的协同作用;TAT-N24有望被开发为有效的白血病分化治疗药物。Objective To investigate the effect of cell-permeable fusion peptide TAT-N24 on the differentiation of acute myeloid leukemia HL60 cell line. Methods HL60 cells were incubated with TAT-N24. The cell morphological changes were observed before determination of the CDllb and CDI4 expressions by flow eytometry. The proliferation ability of the HL60 ceils was determined by BrdU/PI incorporation assay. Results The expressions of CD1 lb and CD14 were both elevated after the TAT-N24 treatment. The morphological features of HL60 cells tend to be like differentiated ceils. Moreover, TAT-N24 could cooperate with all-trans retinoic acid in inducing the differentiation of HL60 cells. Meanwhile, the proliferation of HL60 cells could be inhibited by TAT-N24. Conclusions TAT-N24 could efficiently induce the differentiation of acute myeloid leukemia HL60 ceils, and could inhibit the DNA synthesis of HL60 cells. TAT-N24 could also enhance the efficiency of all-trans retinoic acid in inducing HL60 cell differentiation. TAT-N24 may be potentially developed as an effective medicine for the treatment of the leukemia cell differentiation.

关 键 词:白血病 TAT—N24穿膜融合多肽 HL60细胞株 分化 全反式维甲酸 

分 类 号:R733.7[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象