神经胶质瘤是最常见的神经系统恶性肿瘤，易复发，死亡率高。叉头框转录因子(FOX)基因家族在人类多种恶性肿瘤的进展过程中发挥了重要的作用，而作为其主要成员之一的FOXC2在胶质瘤的发生发展中产生了哪些重要影响仍不清楚。我们的前期结果显示FOXC2在胶质瘤组织及细胞系中表达明显上调；当敲减FOXC2基因后，能明显抑制胶质瘤细胞的增殖、克隆形成、迁移、侵袭、裸鼠成瘤等恶性行为，为了揭示其中具体的分子机制，我们筛选了多个相关基因，并首次发现EphB4/EphrinB2的表达发生了显著变化，并利用Western blot及免疫组化的方法进行验证。本项目旨在进一步明确FOXC2在胶质瘤发生发展中的生物学功能，并阐明FOXC2调控EphB4/EphrinB2转录水平的分子机制，鉴定其基因调控网络，为胶质瘤的治疗提供新的靶点和思路。

Glioma is the most common type of primary central nervous system tumors, and is characterized by high recurrence and mortality rates. In many human cancers, gene family of FOX plays a critical role in tumorigenesis. However, the role and mechanism of FOXC2 in human cancers particularly in glioma remain largely unclear. Our preliminary results show that the expression of FOXC2 is up-regulation in glioma tissues and cell lines. And knockdown of FOXC2 in glioma cell line can inhibit cell proliferation and clone formation, migration and invasion significantly. In order to reveal the molecular mechanism, we found that expression of EphB4/EphrinB2 had a significant change. Thus, the aims of this project are to further explore biological roles and molecular mechanisms of FOXC2 in glioma tumorigenesis at epigenetic regulation, and identify its downstream target genes using ChIP-Seq and RNA-Seq approaches.