基于胶质瘤起源的靶向干预是当前胶质瘤治疗的热点。既往研究表明胶质瘤的形成与神经干细胞（NSCs）神经生成密切相关。新近研究发现源于Hypocretin神经元的神经纤维与室管膜下区（SVZ）保持密切联系，并抑制该区NSCs神经生成。然而Hypocretin神经元与胶质瘤发生进展的关系鲜有报道。本项目中，我们提出Hypocretin神经元可能通过调节SVZ神经生成参与胶质瘤发生发展。为论证上述假设，我们将首先通过动物实验明确Hypocretin神经元对小鼠SVZ内NSCs神经生成以及胶质瘤进展的影响；其次，体外实验中深入分析Hypocretin对NSCs增殖分化和胶质瘤细胞增殖凋亡的影响，以及DACT2信号通路在其中的重要作用；此外，我们还将进一步利用生物信息学数据分析Hypocretin表达水平对胶质瘤患者预后的影响。上述研究将可能为胶质瘤的发生机理提供新的理论依据，为靶向治疗提供新的思路。

Targeted intervention at the level of glioma origin is the key to the current treatment of glioma. Previous studies have shown that glioma is closely related to neurogenesis of neural stem cells（NSCs）. Recent studies have found that fibers of hypocretin neurons project to the subependymal zone（SVZ）, inhibiting the neurogenesis of NSCs, however, the relationship between hypocretin neurons and glioma formation and progression has rarely been reported. In this project, we hypothesized that hypocretin neurons may inhibit the occurrence and progression of glioma through regulating neurogenesis in subventricular zone. To demonstrate this hypothesis, we will first confirm the effects of hypocretin neurons on neurogenesis of NSCs and glioma progression in mice SVZ through animal experiments. Secondly, the effects of hypocretin on proliferation and differentiation of NSCs and proliferation and apoptosis of glioma cells and the changes of specific molecular signaling pathways （DACT2 sigaling) were analyzed in vitro. In addition, we will further analyze the impact of hypocretin expression on the prognosis of glioma patients through clinical and bioinformatics data. These studies may provide a new theoretical basis for the mechanism of glioma and a new idea for targeted therapy.