白血病细胞侵袭力及转移与黏附分子表达的关系  

Correlation between infiltration and metastasis of leukemia cells and adhesion molecules expression

作　　者：李朝霞[1] 王宁遂[1] 杨锡强[1] 徐酉华[1] 李欣[1] 

机构地区：[1]重庆医科大学附属儿童医院,400014

出　　处：《中华儿科杂志》2002年第10期585-588,共4页Chinese Journal of Pediatrics

摘　　要：目的　研究急性白血病 (AL)细胞浸润及转移与黏附分子CD49d表达之间的关系及相应单克隆抗体的阻断效应 ,探讨AL细胞发生浸润和远处转移的分子机理。方法　对 2 0例急性淋巴细胞性白血病 (ALL)和 2 0例急性非淋巴细胞性白血病 (ANLL)患儿 ,采用免疫荧光染色 (IFS)和流式细胞术 (FCM)检测AL细胞表面CD49d的表达水平。采用ELISA和FCM检测体外培养的人脐静脉内皮细胞(HUVEC)经白血病细胞培养上清液或肿瘤坏死因子α(TNF α)作用后细胞间黏附分子 (ICAM 1) ,血管细胞黏附分子 (VCAM 1)的表达水平 ;采用甲基噻唑基四唑 (MTT)法检测AL细胞与HUVEC间黏附率 ,并观察相应单克隆抗体对黏附的抑制作用。结果　 (1)临床浸润明显的ALL和ANLL细胞表面CD49d明显高于正常对照组和非浸润组 (P <0 0 1)。 (2 )HUVEC经AL细胞培养上清液或TNF α刺激后ICAM 1、VCAM 1表达水平均增加 ,但是CD49d高表达的AL细胞与HUVEC之间黏附率随VCAM 1上调而增高 ,与ICAM 1表达无关。结论　AL细胞浸润与表面黏附分子CD49d表达水平有明显关系 ,提示 ,非常晚期抗原 4 (VLA 4 )及配体VCAM 1是AL细胞与血管内皮细胞黏附作用的主要分子基础。使用相应的单克隆抗体可抑制黏附分子间的作用 ,阻断AL细胞的异常生物学行为 ,对防止AL细胞浸润具有一定?Objective Acute leukemia (AL) is the most common cancer and the second leading cause of death in children The AL cells often infiltrate to the central nervous system and other extramedulary organs and cause the relapse of this disease The study here aimed to explore the molecular mechanism of some adhesion molecules to be involved in the infiltration process Methods The adhesion molecule CD 49d , the subunit of very late antigen 4 (VLA 4) expressed in AL cells, was detected by immune fluorescence staining (IFS) and flow cytometry (FCM) Human umbilical vein endothelia cells (HUVECs) were cultured in vitro The ligands, intercellular adhesion molecule 1 (ICAM 1) and vascular cell adhesion molecule 1 (VCAM 1) expressed in HUVECs both before and after stimulating with the supernatant of cultured AL cells or TNF α, were examined by ELISA and FCM Adhesion rates between AL cells and HUVECs were measured by methyl thiazolyl tetrazolium (MTT) method Blocking adhesion rates with different monoclonal antibodies and their combination were tested also by MTT Results The CD 49d expression levels in ALL group and ANLL group with infiltration were 96 48%±5 54% and 95 21%±5 17%, respectively, which was significantly higher than those in non infiltration group and control group ( P <0 01) There was no VCAM 1 expression in HUVECs at the beginning of TNF α stimulation, then the expression increased and reached to the peak level in 12 h (A=0 6) The VCAM 1 expression was paralleled with the adhesion rates between the AL cells and HUVECs Both of them was up to the peak levels after HUVECs were stimulated by TNF α in 12 h The adhesion rate of ANLL cell was 28 6% and the ALL cell was 30 2%, both increased 3 times than that in the un stimulating cells The anti CD 49d or/and anti VCAM 1 monoclonal antibodies markedly reduced the adhesion rates between AL cells and HUVECs (30%～45%) The blocking adhesion rate with all four monoclonal antibodies was 50% Conclus

关 键 词：急性白血病 细胞侵袭力 肿瘤转移 

分 类 号：R733.71[医药卫生—肿瘤]