细胞外信号调节激酶1/2参与三氧化二砷诱导的胶质瘤细胞凋亡  

Extracellular signal-regulated kinase 1/2(ERK1/2) participats in the glioma apoptosis induced by As_2O_3

作　　者：郑天虎[1] 郭庆杰[1] 王福梅[1] 刘兴汉[2] 赵世光[1] 

机构地区：[1]哈尔滨医科大学附属一院神经外科,黑龙江哈尔滨150001 [2]哈尔滨医科大学生化教研室,黑龙江哈尔滨150001

出　　处：《现代肿瘤医学》2006年第11期1341-1344,共4页Journal of Modern Oncology

摘　　要：目的:探讨细胞外信号调节激酶1/2(ERK1/2)信号通路在三氧化二砷诱导的胶质瘤细胞U251凋亡中的作用,为应用三氧化二砷治疗胶质瘤奠定基础。方法:50μmol/L三氧化二砷作用U251细胞,不同时间检测胶质瘤细胞增殖活性,半定量PCR检测ERK1/2mRNA表达,Western blot检测ERK1/2蛋白表达;Ho-echst33258染色及流式细胞术(FCM)检测细胞凋亡;转染ERK1/2上游激酶MEK1,应用ERK1/2激酶抑制剂U0126观察ERK1/2通路在肿瘤凋亡及增殖中的作用;比色分析法检测Caspase-3活性的变化。结果:三氧化二砷诱导胶质瘤细胞发生明显凋亡,抑制肿瘤细胞增殖;增加ERK1/2蛋白的表达,呈时间依赖性;阻断ERK1/2信号通路后胶质瘤细胞凋亡受到抑制,Caspase-3活性下降。结论:ERK1/2信号通路在三氧化二砷诱导的胶质瘤细胞凋亡中起重要作用。Objective：To explore the effects of ERK1/2 in the apoptosis induced by As2 O3. Methods： The glioma cells, U251, was treated with As2O3 （501xmol/L） , the viability of glioma was detected at various time. mRNA and protein of ERK1/2 was detected at various time by RT - PCR and Western blot respectively. Apoptosis was studied using Hoechst 33258 staining and FCMs. The kinase of ERK1/2,MEKI,was transfected in to U251 and the inhibitor of ERK1/2, U0126,was used to study the effects of ERK1/2 in the apoptosis of U251. Colorimetric assay was used to dectected the activity of Caspase - 3. Results ： As2O3 induced apoptosis ,inhibited the proliferation of glioma cells. The protein of ERK1/2 was up - regulated in a time - dependent manner. Apoptosis and activity of caspase - 3 was inhibited by blocking the ERK1/2 signal pathway. Conclusion： ERK1/2 plays an important role in glioma apoptosis induced by As203.

关 键 词：胶质瘤 三氧化二砷 细胞外信号调节激酶1/2 凋亡 

分 类 号：R73-361[医药卫生—肿瘤]