β-1,4-半乳糖基转移酶Ⅴ（β4GalT5）和MTDH均在胶质瘤的发生发展中发挥重要作用，课题组前期研究发现MTDH可与β4GalT5相结合，并提出β4GalT5可通过催化MTDH的N-糖基化修饰，影响MTDH下游基因表达，从而影响胶质瘤发生发展的假说。本课题拟首先证明MTDH存在N-糖基化修饰，并且其N-糖基化可以介导胶质瘤生物学行为的改变；接着证明β4GalT5可与MTDH发生结合，调节MTDH的N-糖基化修饰；然后分析β4GalT5催化MTDH的N-糖基化修饰对MTDH调节的下游基因表达的影响；在此基础上分析β4GalT5催化MTDH的N-糖基化修饰对胶质瘤细胞增殖、迁移及侵袭的影响；最后在临床标本及裸鼠模型中证明β4GalT5催化MTDH的N-糖基化修饰促进胶质瘤的发生及发展。课题研究将为阐明蛋白质糖基化在胶质瘤发生发展过程中的作用和防治的分子靶点提供理论和实验依据。

β4GalT5 and MTDH play important roles in the glioma process. Our previous study has found that β4GalT5 can interact with MTDH, so we hypothesized that β4GalT5 catalytic the MTDH by N-glycosylation modification and affect the glioma process through regulating the MTDH tageting gene expression. In our present work, we intend to prove that the MTDH undergoes a N-glycosylation modification which plays a role in the glioma process. Then, we will investigate that β4GalT5 interacts with MTDH and thus catalytic its N-glycosylation. Afterwards, we will detect the gene expression regulated by MTDH under the condition of N-glycosylation catalytic by β4GalT5. Next, we will check the effects on the glioma cells proliferation, migration and invasion. Finally, we will validate the works in the clinical specimens and animal models. Our study will provide the experimental and theoretical basis for elucidating the pathogenesis of the glioma, and a new therapeutic taget for the glioma treatment.