摘要
目的探讨多配体蛋白聚糖结合蛋白（Syntenin）促进脑胶质瘤迁移和侵袭过程的分子机制。方法应用RT-PCR技术和免疫印迹方法研究84例不同病理级别人脑胶质瘤组织中Syntenin与磷酸化FAKTyr397基因和蛋白的表达情况，比较二者与胶质瘤分级的关系以及表达的相关性。结果RT-PCR检测结果显示，Syntenin mRNA和FAK mRNA表达水平在各级胶质瘤组织之间均存在明显差异（P〈0．05），二者表达水平的上调均与肿瘤级别的增加呈正相关（rSyntenin=0．91，P〈0．05；r FAK=0．97，P〈0．05）；免疫印迹结果发现，Syntenin和磷酸化FAKTyr397的表达在各级胶质瘤组织中存在差异（P〈0．05）；其表达水平均随胶质瘤病理级别的增加而上调（rSyntenin=0．91，P〈0．05；rFAK=0．90，P〈0．05）；Syntenin表达水平的提高与FAK Tyr397的磷酸化水平呈正相关（r=0．90，P〈0．05）。结论脑胶质瘤细胞中Syntenin可能通过与FAK相互作用经相应的信号转导途径增加脑胶质瘤细胞迁移和侵袭的能力。
Objective To investigate the molecular mechanism of Syntenin in the enhancement of migration and invasion of brain gliomas. Methods We investigated the expression levels of Syntenin mRNA and FAK mRNA with reverse transcription - polymerase chain reaction （RT- PCR ）, and verifed the expression levels of Syntenin and phosphorylated FAK Tyr397 with immunoblot in 84 cases of human brain gliomas. Its correlation to the pathologic grade, and the relationship between the expression of Syntenin and phosphorylated FAK Tyr397 in human brain gliomas were studied. Results There were significant differences （ P 〈 0. 05 ） in the expression of Syntenin mRNA and FAK mRNA in glioma tissues by RT - PCR. The increasing expression levels of Syntenin mRNA and FAK mRNA had positive correlation with the ascending of pathologic grade of tumor specimen （ r Syntenin = O. 91, P 〈 O. 05, r FAK = O. 97, P 〈 O. 05 ）. The results of immunoblot showed that there were significant differences （ P 〈 O. 05） in the expression of Syntenin and phosphorylated FAK Tyr397 in glioma tissues. With the ascending of pathologic grade of tumor specimens, the expression levels of Syntenin and phosphorylated FAK Tyr397 protein increased markedly（ r Syntenin =0. 91, P 〈 0. 05; r FAK =0. 90, P 〈 O. 05）. There was positive correlation betwenn the expression level of phosphorylated FAK Tyr397 and Syntenin in gliomas （ r = 0. 90, P 〈 0. 05 ）. Conclusion The invasion and migration ability of glioma might be enhanced by Syntenin though its interaction with FAK in a corresponding signal transduction pathway.
出处
《中华神经外科杂志》
CSCD
北大核心
2014年第3期305-308,共4页
Chinese Journal of Neurosurgery
基金
重庆市科委自然科学基金科研项目（cstc2011jjA10091）
财政部、卫生部国家临床重点专科建设项目[财社（2001）170号]
