bcl-2在HL-60细胞分化和凋亡过程中的表达  

Expression of bcl-2 during Differentiation and Apoptosis of HL-60 Cells

作　　者：曾辉[1] 赵相印[1] 赵如冰[2] 刘复强[1] 杨敏[1] 马雅銮[2] 鞠淑英[1] 王瑾[1] 高天祥[2] 

机构地区：[1]首都医科大学附属北京同仁医院血液科,北京100730 [2]首都医科大学分子生物学实验室,北京100054

出　　处：《中国实验血液学杂志》1997年第4期372-377,共6页Journal of Experimental Hematology

摘　　要：细胞凋亡抑制基因bcl-2在髓系造血细胞中的表达与细胞分化程度有关。本研究证实全反式维甲酸(ATRA)可诱导HL-60细胞凋亡。流式细胞仪分析表明,在HL-60细胞分化凋亡过程中bcl-2表达逐渐下降,凋亡细胞bcl-2表达水平较低,而未凋亡细胞bcl-2仍维持在高水平。上述结果提示:经ATRA诱导分化成熟的HL-60细胞与正常粒细胞相似,最终走向凋亡;bcl-2表达降低可能对终末分化细胞凋亡有易化作用;未凋亡细胞bcl-2高表达可能是肿瘤细胞耐药和白血病复发的重要因素。The bcl-2 oncogene expression is differentiation-linked in normal myeloid cells. In the present study, HL-60 cells treated by all-trans retinoic acid (ATRA) underwent apoptosis following terminal differentiation. Flow cytometric analysis revealed that bcl-2 oncoprotein was down-regulated during differentiation and apoptosis process. Significant reduction of bcl-2 level was noted in the apoptotic cells, while the non-apoptotic cells remained a relatively high level of bcl-2. The results suggest that ATRA may initiate apoptosis in morphologically mature HL-60 cells after inducing irreversible commitment to differentiation. Like in normal neutrophils, down-regulation of bcl-2 expression appears to facilitate apoptosis in differentiated HL-60 cells. High level of bcl-2 in the non-apoptotic cells may play an important role in drug-resistance and leukemia relapse.

关 键 词：HL-60细胞 细胞分化 细胞凋亡 BCL-2基因 全反式维甲酸 

分 类 号：R329[医药卫生—人体解剖和组织胚胎学]