表皮生长因子受体阻断对前列腺癌细胞增殖的影响  

Inhibition of proliferation by blockade of epidermal growth factor receptor in human prostate carcinoma cells

作　　者：叶定伟[1] 李慧[2] JaneTseng PriscillaChauvin 钱松溪[1] 孙颖浩[1] 郑家富[1] 马永江[1] 

机构地区：[1]第二军医大学长海医院泌尿外科,上海200433 [2]第二军医大学长海医院内分泌科,上海200433 [3]UTMDAndersonCancerCenter

出　　处：《中华实验外科杂志》2002年第4期360-361,共2页Chinese Journal of Experimental Surgery

摘　　要：目的　探讨阻断表皮生长因子受体 (EGFR)对前列腺癌 (PCa)细胞增殖的影响。方法　人PCa细胞株DU 14 5 ,分别加或不加抗EGFR单抗C2 2 5 (2 0nmol/L)阻断EGFR体外细胞培养 7d ,收集细胞、计数以观察对PCa雄激素非依赖增殖的影响 ,并采用免疫沉淀和Westernblot方法 ,探讨阻断EGFR后不同时相点磷酸化有丝分裂原激活下蛋白激酶MAPK ,及 p2 7kip1的表达变化。结果　阻断EGFR与对照相比较可使DU 14 5细胞增殖被抑制达 3 5 % ,8h后磷酸化MAPK的表达水平开始降低 ,p2 7kip1表达开始升高 ,至 2 4h最明显。结论　阻断EGFR可抑制PCa细胞增殖 ,可能的机制是MAPK的活性降低 ,使 p2 7kip1的表达升高而细胞周期被阻。Objective To investigate the inhibition of proliferation by blockade of epidermal growth factor receptor (EGFR) and the activation of MAPK and expression of p27 kip1 in prostate carcinoma cells.Methods In human androgen independent prostate carcinoma cell line DU 145,the cell proliferation was measured by cell culture in vitro for 7 days in the presence or absence of the monoclonal antibody against EGFR.Expression of phosphorylated MAPK and p27 kip1 was detected by using immunoprecipitation and Western Blot analysis after treatment of anti EGFR antibody for 0,8,16 and 24 h.Results The proliferation of DU 145 cells was inhibited by 35% after treatment of anti EGFR antibody for 7 days as compared with the controls.The level of phosphorylated MAPK was down and the p27 kip1 was up after treatment of anti EGFR antibody for 8 h and it was the most significant after 24 h.Conclusion Blockade of EGFR could prohibit the proliferation of prostate carcinoma cells,which was contributed to the decreased activation of MAPK to upregulate the p27 kip1 and arrest cell cycle.

关 键 词：表皮生长因子受体 前列腺癌 细胞增殖 细胞周期 

分 类 号：R737.25[医药卫生—肿瘤]