胶质母细胞瘤是中枢神经系统最常见的原发恶性肿瘤，可分为不同的亚型而呈现鲜明的肿瘤内异质性。其他亚型向恶性度更高的间质型的转化是胶质母细胞瘤恶性进展的重要指标，即上皮间质转化。上皮间质转化相关分子靶向治疗是目前的热门研究。EID3是CBP/P300的抑制物家族的分子之一，我们前期研究发现EID3的表达显著影响胶质母细胞瘤预后，并且EID3可以调控胶质母细胞瘤的上皮间质转化过程，并且和EID3与HDAC1的相互作用调节下游NF-κB通路有关。在此基础上，我们拟开展更深入的研究EID3如何通过HDAC1来影响胶质母细胞瘤上皮间质转化过程，以揭示EID3影响胶质母细胞瘤的肿瘤生物学功能的分子机制。本项目所涉及研究内容，以阐明EID3在胶质母细胞瘤中的促癌作用，为EID家族与组蛋白去乙酰化、核受体因子之间关系奠定基础，并为靶向抑制EID3作为治疗胶质母细胞瘤做出理论依据。具有十分重要的理论意义。

Glioblastoma multiforme (GBM) is the most common primary malignant tumor in central nervous system.GBM showed obvious intra-tumor heterogeneity based on molecular or genetic changes among different subgroups. Different subgroups of GBM can transform into mesenchymal subgroup, which refers to malignant progression, greater chemotherapy resistance and worse prognosis. This process is called the epithelial-mesenchymal transition (EMT). EMT related molecular targeted therapy is currently a hot research field for the treatment of GBM. EP300 inhibitor differentiation 3 (EID3) is one of the inhibitors of CBP/P300, which has been found to be related to tumorigenesis and tumor development. Our previous studies found that the expression of EID3 was related to the grading, developing and prognosis in GBM, and that EID3 could participate in the EMT process of GBM. In addition, the multiple functions of EID3 on GBM were shown to be related to the interaction with HDAC1 and regulation of the downstream NF-κB pathway. In the project, we plan to conduct further researches to reveal how EID3 affects the tumor biological function of GBM; how EID3 affects the EMT process of GBM through the interaction with HDAC1. It will elucidate the function of EID3 in GBM, and lay the foundation for the relationship between the EID family and histone deacetylation activity during EMT process. It has very important theoretical significance toward targeted inhibition of EID3 as a theoretical basis for the treatment of GBM.