论文部分内容阅读
目的:探讨生殖细胞特异基因-2(GSG2)基因在神经胶质瘤中的作用。方法:通过慢病毒敲除GSG2的U87细胞系构建裸鼠成瘤模型。随后进行瘤体体积、重量测量和动物活体成像分析，并应用蛋白芯片技术探讨下游分子机制。采用非配对n t检验或n χ2检验来计算两组之间的差异。n 结果:GSG2敲低后1个月裸鼠瘤体明显减小[敲低(KD)组：(109.42±209.94) mmn 3，对照(NC)组：(1 070.00±410.28) mmn 3，n P<0.05]，凋亡相关蛋白Fas、Fas配体(FasL)、p27、p53、SMAC的表达水平显著上调(n P<0.05)，SMAC蛋白激活最为明显。n 结论:GSG2在体内促进神经胶质瘤细胞凋亡，并降低胶质瘤增殖。“,”Objective:To study the role of germ cell specific gene 2 (GSG2) gene in glioma.Methods:The tumor-forming model of nude mice was established by deletion of GSG2 U87 cell line by lentivirus. Subsequently, tumor volume, weight measurement and n in vivo animal imaging analysis were carried out, and the downstream molecular mechanism was discussed by using protein chip technology.n Results:After GSG2 was knocked down, the tumor size of nude mice was significantly reduced [KD group: (109.42±209.94) mmn 3, NC group: (1 070.00±410.28) mmn 3, n P<0.05], the expression levels of apoptotic proteins Fas, Fas ligand (FasL), p27, p53 and SMAC were significantly up-regulated (n P<0.05), and the activation of p53 was the most obvious.n Conclusion:GSG2 promotes p53 mediated apoptosis of glioma cells n in vivo and reduces glioma proliferation.n