胶质瘤是最常见的颅内恶性肿瘤。糖皮质激素受体β（GRβ）是我们新鉴定的胶质瘤促癌因子，但其高表达机制尚未明确。我们前期工作提示这可能与RNA剪接蛋白SRSF9介导的GR基因mRNA的选择性剪接有关。RNA的异常剪接在肿瘤组织中广泛存在，我们前期研究发现SRSF9在胶质瘤中高表达，且高表达患者生存期更短，体外功能实验提示其是胶质瘤的一个潜在促癌因子。初步的机制研究显示SRSF9不仅调控GRβ表达，而且介导凋亡相关分子BCL-XL的选择性剪接，发挥抗凋亡作用。据此我们推测SRSF9介导的RNA选择性剪接在胶质瘤发生发展中发挥重要作用。本课题将通过组织、细胞和动物水平的研究，结合高通量转录组测序及RIP-seq技术，解析SRSF9在胶质瘤中的作用及分子机制，以期从RNA剪接调控水平上探讨胶质瘤的发病机理，为胶质瘤的防治提供新靶点和新思路。

Glioma is the most common and highly lethal type of primary brain cancer. Previous studies have documented that GRβ (glucocorticoid receptor β) serves as a tumor promoting factor in glioma. In the present study, we found alternative splicing factor SRSF9 may regulate alternative splicing of GR mRNA and enhance GRβ expression. Aberrant alternative splicing may be a significant but yet under-explored contributor to heterogeneous pathological characteristics of malignant tumor. We found that SRSF9 was upregulated in human gliomas, and there was a highly significant correlation between SRSF9 and overall survival of patients. In vitro assays demonstrated that SRSF9 is a potential glioma cancer promoting factor, and GRβ was regulated by SRSF9. Further study showed that SRSF9 mediates the anti-apoptotic effect by regulating the alternative splicing of another target gene BCL-XL. According to these results, we proposed that alternative splicing mediated by SRSF9 may play an important role in the development of glioma. The present study will investigate the function and mechanisms of SRSF9 in glioma, by using glioma tissues, cellular biology techniques and animal models, combined with high throughput transcriptome sequencing and RIP-sequence. We hope this study will enrich our knowledge of glioma pathogenesis at the splicing regulation level and provide novel strategies and potential therapeutic targets for malignant glioma treatment.