中文摘要：

目的探讨鼻咽癌中PTTG1与MAPK／ERK信号通路及细胞增殖凋亡的关系。方法采用免疫组化sP法检测33例鼻咽癌中PTFGl、p-ERK、Ki-67蛋白的表达；用50、100μmol／L的ERK／MAPK信号传导通路抑制剂PD98059，分别处理CNE-2Z细胞24、48、72h，免疫细胞化学法检测PTTG1、P—ERK、Ki-67蛋白的表达；MTT法检测细胞增殖抑制率；流式细胞仪检测细胞凋亡。结果33例鼻咽癌组织中PTTG1、p-ERK、Ki-67蛋白的阳性表达率分别为81．82％（27／33）、66．67％（22／33）、78．79％（26／33）；PTTG1与P—ERK（r=0．345，P=0．042〈0．05）、Ki-67（r=0．600，P〈0．01）蛋白表达均呈正相关；不同浓度PD98059作用于CNE-2Z细胞不同的时间，免疫细化检测PTTG1、p-ERK、Ki-67蛋白的阳性表达降低，细胞增殖明显受抑制，可检测到凋亡峰。结论PTTG1在鼻咽癌中可能通过MAPK／ERK信号通路发挥促进癌细胞增殖及抑制凋亡的生物学作用。

英文摘要：

Objective To investigate the relationship between VI＇TG1 and MAPK/ERK signalpathway, proliferation, apoptosis in nasopharyngeal carcinoma （NPC）. Methods Immunohistochemistry SP method was adopted to detect the ex- pression of PTTG1, p-ERK, Ki-67 protein in 33 cases NPC. CNE-2Z cells was treated with different dose of ERK/MAPK signal way inhibitors PD98059 （50 μmol/L, 100 μmol/L）, and immunohistochemistry SP method was adopted to detect the expression of PTrG1, p-ERK, Ki-67 protein, MTT was adopted to detected proliferation, flow cytometry was used to observe apoptosis. Results Positive staining rates of PTYG1, p-ERK, Ki-67 protein in 33 cases NPC was 81.82% （27/ 33 ）, 66.67% （ 22/33 ）, 78.79% （ 26/33 ）, respectively. There was statistically significant positive correlations between positive expression of PTI＇G1 and p-ERK （ r = 0.345, P 〈 0.05）, Ki-67 （ r = 0. 600, P 〈 0.01 ） protein. When CNE-2Z cells treated by different time and different dose of PD98059, the expression of PTTG1, p-ERK, Ki-67 protein was decreased, CNE-2Z cellular proliferation was restrained remarkably, apoptosis can be observed. Conclusion PTTG1 may play biology effect through MAPK/ERK signal pathway promoting cellular proliferation and inhibiting apoptosis in NPC.