CRKL活性与白血病细胞多药耐药的关系  

Study on the relationship between CRKL activity and multidrug resistance in leukemia cell lines

作　　者：沈绍华[1] 亓春花[1] 顾龙君[2] 杨宪勇[1] 叶欣[1] 

机构地区：[1]山东省泰安市中心医院儿科,271000 [2]上海交通大学附属新华医院上海儿童医学中心血液肿瘤科

出　　处：《白血病．淋巴瘤》2009年第7期385-387,391,共4页Journal of Leukemia & Lymphoma

摘　　要：目的探讨CRKL活性在白血病细胞多药耐药中的作用，发现与耐药相关的新因素。方法应用流式细胞术比较CRKL在K562、HL-60及其耐药细胞中的活性变化；对敏感细胞用柔红霉素处理后，检测CRKL活性与化疗作用时间的关系以及撤药后CRKL活性的改变。结果与K562、HL-60敏感细胞比较，在K562、HL-60耐药细胞株中，CRKL的磷酸化水平明显升高；在用柔红霉素处理72h后，K562和HL-60细胞CRKL的磷酸化水平与化疗药物作用呈时间依赖性，未发现Jurkat细胞CRKL磷酸化水平的改变。结论CRKL活性变化与白血病细胞多药耐药的形成有关，是白血病细胞多药耐药的又一个新的影响因素。Objective To investigate the role of CRKL activity in leukemia cells with muhidrug resistance and find new factor related to muhidrug resistance. Methods By flow cytometry, CRKL activity was compared in K562, HL-60 cells and its resistance cells. The change of CRKL activity was observed in sensitive cells treated with and withdrawal daunorubicin. Results With the comparison of K562, HL-60 sensitive cells, in K562, HL-60 resistant cell lines, the level of CRKL phosphorylation in K562, HL-60 resistance cells treated with daunorubicin 7：2 hours increased markedly. The level of CRKL phosphorylation was time-dependent with chemotherapy drugs, not change of CRKL activity was found in Jurkat cells. Conclusion The level of CRKL activity is new factor related to muhidrug resistance in leukemia cells.

关 键 词：白血病 原癌基因 磷酸化酶类 

分 类 号：R733.7[医药卫生—肿瘤] R733.72[医药卫生—临床医学]