Gefitinib对前列腺癌DU145细胞EGFR、MAPK、AKt及PKC蛋白表达的影响  

Expressions of EGFR, MAPK, AKt and PKC in prostate cancer cells DU 145 treated with Gefitinib

作　　者：陈永昌[1] 张杰[1] 付振宇[1] 张鸽[1] 马俊[1] 陈卫国[2] 张庆磊[2] 

机构地区：[1]常熟市第二人民医院,常熟215500 [2]苏州大学附属第一医院泌尿外科

出　　处：《中国男科学杂志》2013年第4期24-25,29,共3页Chinese Journal of Andrology

摘　　要：目的探讨在Gefitinib 作用下前列腺癌DU145细胞表皮生长因子受体（EGFR）、促分裂原活化蛋白激酶（MAPK）、丝氨酸蛋白激酶（AKt）及蛋白激酶C（PKC）蛋白表达水平的变化.方法使用终浓度为10μmol/L Gefitinib体外作用于DU145细胞,Western blot检测DU145细胞EGFR、MAPK、AKt、PKC蛋白表达水平.结果 经Gefitinib作用后DU145细胞EGFR、Akt蛋白水平分别降低了69.57%和58.31%,而MAPK及PKC 蛋白分别仅降低35.93%和32.7%.结论 Gefitinib作用后DU145细胞发生生长抑制可能和EGFR、Akt蛋白表达抑制有关,而和MAPK及PKC蛋白抑制无关.Objective To investigate the inhibitory effects of Gefitinib on the growth of DU145 cells and their expressions of EGFR, MAPK, AKt and PKC. Methods DU145 cells were treated with 10μmol/L Gefitinib in vitro. The expression of EGFR, MARK, Akt and PKC were detected by Western blot. Results Compared with that of the control group, EGFR and Akt protein level in the treated DU145 cells were decreased 69.57% and 58.31% respectively, while MAPK and PKC protein level were decreased 35.93% and 32.7% respectively. Conclusion Obvious downregulation of EGFR and Akt in the treated DU145 cells obviously might inhibit tumor cell growth and reduce proliferative activity of cells.

关 键 词：吉非替尼 前列腺肿瘤 受体 表皮生长因子 蛋白激酶类 

分 类 号：R737.25[医药卫生—肿瘤]