HIV-1反式激活蛋白介导的白血病抑制因子受体α亚基胞内区远膜端融合蛋白在HL-60细胞分化中对microRNA-155的影响  

Effect of TAT-mediated LIF receptor α-chain distal cytoplasmic fusion protein on microRNA-155 in the differentiation process of HL-60 cells

作　　者：徐莎[1] 许震宇[1] 王越[1] 刘厚奇[1] 

机构地区：[1]第二军医大学组织学与胚胎学教研室,上海200433

出　　处：《解剖学杂志》2014年第4期454-457,共4页Chinese Journal of Anatomy

摘　　要：目的：探讨HIV-1反式激活蛋白（TAT）与白血病抑制因子（LIF）受体α亚基胞内区C末端序列（LIFRα-CT3）的融合蛋白（TAT-CT3）,对HL-60细胞分化的影响.方法：将HL-60细胞分为对照组和TAT-CT3组.流式细胞仪对HL-60细胞进行粒细胞表面分化标记物CD14、CD11b的检测;Real-time PCR检测HL-60细胞中BIC、miR-155及其下游靶基因C/EBP β和SOCS-1 mRNA的表达;免疫印迹检测HL-60细胞中C/EBP β、SOCS-1及pSTAT3蛋白的表达.结果：与对照组相比,TAT-CT3组的HL-60细胞,其粒细胞表面分化标记物CD14、CD11b阳性表达率增加;BIC、microRNA-155（miR-155）表达量降低,C/EBP β和SOCS-1 mRNA及蛋白表达量均增加,pSTAT3蛋白表达量降低.结论：TAT-CT3融合蛋白通过抑制miR-155的表达,促进HL-60细胞向成熟粒细胞方向分化.Objective：To investigate the effect of TAT-CT3 fusion protein on the differentiation of HL-60 cells.Methods：HL-60 cells were divided into a control group and TAT-CT3 group.The cell surface marker CD14 and CD11b were detected by flow cytometer after 4 days.The expressions of BIC,microRNA-155 （miR-155）,C/EBP β and SOCS-1 mRNA were examined by real-time PCR and the expression of C/EBP β,SOCS-1 and phosphorylated STAT3 protein were examined by Western blotting analysis.Results：Compared with the control group,4 days later the TAT-CT3 group had a higher positive rate of CD14 and CD11b.The expressions of BIC and miR-155 were depressed,with an increase of C/EBPβ and SOCS-1 in mRNA and protein level.Moreover,phosphorylated STAT3 was decreased in the TAT-CT3 group.Conclusion：TAT-CT3 fusion protein promotes the differentiation of HL-60 cells by inhibiting the expression of miR-155.

关 键 词：白血病抑制因子受体 HIV-1反式激活蛋白融合蛋白 HL-60细胞 microRNA-155 

分 类 号：R979.1[医药卫生—药品]