丝裂原活化蛋白激酶信号转导系统对Vp-16诱导分化作用的影响  

Mitogen-activated protein kinases signaling mediates etoposide-induced differentiation in chronic myelogenous leukemic K562 cells

作　　者：王甦[1] 刘云鹏[1] 侯科佐[1] 罗颖[1] 刘世洲[1] 

机构地区：[1]中国医科大学附属第一医院肿瘤内科,辽宁沈阳110001

出　　处：《肿瘤防治杂志》2005年第24期1847-1849,共3页China Journal of Cancer Prevention and Treatment

基　　金：辽宁省自然科学基金(20022077);辽宁省教育厅基金(20122152)

摘　　要：目的:探讨丝裂原活化蛋白激酶(mitogen-acti-vated protein kinases,MAPKs)信号转导系统对依托泊苷(Vp-16)诱导K562细胞分化作用的影响.方法:采用四甲基偶氮唑盐(MTT)法测定细胞增殖活性;流式细胞仪解析细胞周期;硝基四氮唑蓝(NBT)还原实验检测细胞向单核/巨噬系统分化.结果:0.1～0.8μg/mL的Vp-16抑制K562细胞增殖,引起细胞G2/M期阻滞,诱导细胞向单核/巨噬系统分化;细胞外信号调节激酶(extracellular signal-regulated kinases,ERK)抑制剂PD98059降低Vp-16的诱导分化作用,P＜0.05;p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kina-ses,p38 MAPK)抑制剂SB203580增强Vp-16的作用,P＜0.05;而C-JUN氨基末端激酶(c-jun N-terminal ki-n2ses,JNK)抑制剂SP600125对Vp-16的诱导分化作用无明显影响,P＞0.05.结论:在Vp-16诱导K562细胞向单核/巨噬系统分化过程中,ERK正向,p38MAPK负向调节Vp-16的诱导分化作用.To explore the effects of Mitogen-activated Protein Kinases on etoposide-induced differentiation in K562 cells. METHODS： The growth inhibition was determined by MTT assay; cell cycle was analysed by the flow cytometry; cell differentiation was measured by nitro blue tetrazoliurn （NBT） reduction test. RESULTS： Etoposide inhibited the proliferation and induced G2/M phrase arrest and differentiation toward monocyte/rnacrophage-like cells of K562 cells. Extracdlular signal-regulated kinase （ERK） inhibitor PD98059 decreased the differentiation by Vp-16, P〈0. 05; p38 Mitogen-Activated Protein Kinase （p38MAPK） inhibitor SB203580 increased the action of Vp-16, P〈0. 05;c-jun N-terminal kinase （JNK）inhibitor SP600125 did not affect the action of etoposide, P〉0.05. CONCLUSIONS：In the process of etoposide-induced differentiation toward monocyte/rnacrophage- like cells in K562 cells, ERK pathway positively and p38MAPK pathway negatively regulates the action of etoposide.

关 键 词：丝裂原激活蛋白激酶类 白血病 细胞系 依托泊苷 

分 类 号：R73-36[医药卫生—肿瘤]