Epratuzumab治疗Burkitt's淋巴瘤的分子机制  

Molecular mechanisms of Burkitt's lymphoma treated by Epratuzumab

作　　者：王巍[1] 赵成海[1] 

机构地区：[1]中国医科大学基础医学院病理生理教研室,辽宁沈阳110001

出　　处：《现代肿瘤医学》2011年第11期2188-2190,共3页Journal of Modern Oncology

基　　金：辽宁省自然科学基金项目(编号:20092125);辽宁省教育厅高等学校科研项目(编号:2009A751)

摘　　要：目的:检测抗CD22抗体Epratuzumab对Burkitt's淋巴瘤Raji细胞系表型的影响,及其作用的分子机制。探讨其治疗对Burkitt's淋巴瘤的作用。方法:采用流式细胞技术检测Epratuzumab作用前后Burkitt's淋巴瘤Raji细胞系细胞的凋亡和细胞周期。western-blot技术筛选可能的信号传导通路。结果:Epratuzumab作用后的细胞,可以检测到细胞凋亡增加,G1期阻滞。SHIP,Grb-2,Shc磷酸化程度增高。结论:Epratuzum-ab能通过CD22,介导胞浆内相应蛋白磷酸化,促进Raji细胞系凋亡,抑制其分化,从而达到治疗Burkitt's淋巴瘤的目的。Objective：To study the expression and molecular mechanisms of Raji cell line after treated by Epratuzumab,an antibody of CD22.To discuss the effection on Burkitt＇s leukoma.Methods： Flow cytometry was used to test cell apoptosis and cell cycle of Raji cell line treated by Epratuzumab.To detect the signal pathway using western-blot.Results： After treatment by Epratuzumab cell apoptosis was leveled up and cell cycle was blocked at G1 phase.The phosphorylation of protein SHIP,Grb-2,Shc was higher.Conclusion： Epratuzumab can effect on CD22 that lead to phosphorylation of related proteins.Then advance Raji cell line apoptosis and repress its differentiation.

关 键 词：EPRATUZUMAB CD22 RAJI细胞 

分 类 号：R733.4[医药卫生—肿瘤]