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PTTG1、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、72 h,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PT-TG1、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。
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.
出处
《山东医药》
CAS
2012年第40期1-3,7,共4页
Shandong Medical Journal
基金
国家重点基础研究发展计划(973计划)(2011CB504800)
广东省湛江市科技攻关项目[湛科(2004)90号]
关键词
鼻咽肿瘤
垂体瘤转化基因
细胞外信号调节激酶
增殖
凋亡
nasopharyngeal neoplasm
pituitary tumor transforming gene
extracellular-signal regulated protein Ki-nase
proliferation
apoptosis
