胶质瘤是最常见、预后较差的恶性脑肿瘤，其发生发展机制尚不明确。β-Catenin作为一个重要的原癌基因，能够促进胶质瘤的侵袭。我们前期的研究发现：β-catenin在经典Wnt活化之外的新通路，即PomGnT1/ RPTPβ/β-catenin磷酸化激活通路。但是其中具体的调节机制尚未明确。本项目拟在前期研究上，进一步从分子水平探讨PomGnT1调控RPTPβ/β-catenin磷酸化的机制: PomGnT1通过糖基化作用引起RPTPβ中的HNK-1抗原增加，从而使得RPTPβ胞外段与Galectin-1的结合增加；同时RPTPβ由单体形式变成二聚体，最终导致RPTPβ去磷酸化功能被抑制。而PomGnT1作为葡萄糖氨转移酶，只在哺乳动物中的神经和骨骼肌细胞中发挥作用，是胶质瘤良好的潜在治疗靶点。通过完善上述分子机制，能够为胶质瘤治疗提供新的靶点。

Glioma is the most common malignant brain tumors with the worst prognosis,and the development of its mechanism is not clear. β-Catenin as an important proto-oncogenes promotes glioma invasion. Our previous studies have found that, the new β-catenin pathway in addition to the classical Wnt activation, namely PomGnT1 / RPTPβ / β-catenin phosphorylation pathway activation. But the detail regulatory mechanisms is not yet clear. So the project further to explore the regulation PomGnT1 RPTPβ / β-catenin phosphorylation mechanisms at the molecular level: PomGnT1 increases the HNK-1 peptide of RPTPβ, which makes the extracellular segment of RPTPβ increased binding to galectin-1; while RPTPβ by monomeric form into dimers, further lead RPTPβ dephosphorylated function inhibited. PomGnT1 as glycosyltransferase, only plays a role in mammalian nerve and skeletal muscle cells,.So it is the potential therapeutic target for glioma. This project would provide a scientific basis for the targeted treatment of glioma from the molecular mechanism.