我们前期研究发现人胶质瘤中高表达的糖皮质激素受体β（GRβ）是影响胶质瘤细胞增殖和迁移的重要因素，提示GRβ可能是胶质瘤的一个新促癌基因。目前已知β-catenin信号通路过度活化与胶质瘤的发生发展密切相关，但胶质瘤中β-catenin过度活化的机制尚未明确。我们已有研究表明星形胶质细胞损伤后GRβ能与β-catenin相互作用并增强后者转录调控活性，但胶质瘤中高表达的GRβ是否与β-catenin的高活性存在关联还需进一步明确。据此，我们提出本课题的假说：胶质瘤中GRβ与β-catenin结合并维持β-catenin的高活性，从而促进胶质瘤细胞的增殖、迁移等恶性生物学特性。为验证该假设，本课题拟通过体内、外实验探讨GRβ在胶质瘤发生发展中的生物学功能及其作用机理，重点研究GRβ调控β-catenin活性影响胶质瘤细胞增殖和迁移的分子机制，以期为胶质瘤的防治提供理论和实验依据。

Our recent research determined that elevated glucocorticoid receptor β (GRβ) expression in glioma cells is important for the regulation of cellular proliferation and migration in human glioma, which suggests that GRβ could be a possible glioma oncogene. The high activity of β-catenin is closely related with glioma development, however, the mechanism of β-catenin high activity in gliomas is not clear. Another study in our lab showed that increasing transcriptional regulation ability of β-catenin through the combination of β-catenin and GRβ is the primary factor in glial activation following injury.While, there is no evidence whether the high expression of GRβ in glioma cells is associated with the high activity of β-catenin. Accordingly, we propose our hypothesis: The maintenance of increased β-catenin activity through its binding to GRβ can promote proliferation, migration, and other biological characteristics of malignant glioma. To verify this hypothesis, a series of experiments both in vitro and in vivo will be conducted to investigate the biological function and mechanism of GRβ in glioma development, especially the mechanism of how GRβ affects the activity of β-catenin in the regulation of proliferation and migration of glioma cells. This study will provide theoretical and experimental evidence for the prevention and treatment of human gliomas.