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Abstract：
BACKGROUND: Glioblastoma (GBM) is a highly aggressive and prevalent brain tumor that poses significant challenges in treatment. SRSF9, an RNA-binding protein, is essential for cellular processes and implicated in cancer progression. Yet, its function and mechanism in GBM need clarification.
METHODS: Bioinformatics analysis was performed to explore differential expression of SRSF9 in GBM and its prognostic relevance to glioma patients. SRSF9 and CDK1 expression in GBM cell lines and patients\' tissues were quantified by RT-qPCR, Western blot or immunofluorescence assay. The role of SRSF9 in GBM cell proliferation and migration was assessed by MTT, Transwell and colony formation assays. Additionally, transcriptional regulation of CDK1 by SRSF9 was investigated using ChIP-PCR and dual-luciferase assays.
RESULTS: The elevated SRSF9 expression correlates to GBM stages and poor survival of glioma patients. Through gain-of-function and loss-of-function strategies, SRSF9 was demonstrated to promote proliferation and migration of GBM cells. Bioinformatics analysis showed that SRSF9 has an impact on cell growth pathways including cell cycle checkpoints and E2F targets. Mechanistically, SRSF9 appears to bind to the promoter of CDK1 gene and increase its transcription level, thus promoting GBM cell proliferation.
CONCLUSIONS: These findings uncover the cellular function of SRSF9 in GBM and highlight its therapeutic potential for GBM.
METHODS: Bioinformatics analysis was performed to explore differential expression of SRSF9 in GBM and its prognostic relevance to glioma patients. SRSF9 and CDK1 expression in GBM cell lines and patients\' tissues were quantified by RT-qPCR, Western blot or immunofluorescence assay. The role of SRSF9 in GBM cell proliferation and migration was assessed by MTT, Transwell and colony formation assays. Additionally, transcriptional regulation of CDK1 by SRSF9 was investigated using ChIP-PCR and dual-luciferase assays.
RESULTS: The elevated SRSF9 expression correlates to GBM stages and poor survival of glioma patients. Through gain-of-function and loss-of-function strategies, SRSF9 was demonstrated to promote proliferation and migration of GBM cells. Bioinformatics analysis showed that SRSF9 has an impact on cell growth pathways including cell cycle checkpoints and E2F targets. Mechanistically, SRSF9 appears to bind to the promoter of CDK1 gene and increase its transcription level, thus promoting GBM cell proliferation.
CONCLUSIONS: These findings uncover the cellular function of SRSF9 in GBM and highlight its therapeutic potential for GBM.
摘要：
背景：胶质母细胞瘤（GBM）是一种高度侵袭性和普遍性的脑肿瘤，对治疗提出了重大挑战。SRSF9，一种RNA结合蛋白，对细胞过程至关重要，并与癌症进展有关。然而，其在GBM中的功能和机制有待澄清。
方法：进行生物信息学分析，以探讨SRSF9在GBM中的差异表达及其与胶质瘤患者预后的相关性。通过RT-qPCR定量GBM细胞系和患者组织中的SRSF9和CDK1表达，蛋白质印迹或免疫荧光测定。MTT法评价SRSF9在GBM细胞增殖和迁移中的作用,Transwell和集落形成测定。此外,使用ChIP-PCR和双荧光素酶测定法研究了SRSF9对CDK1的转录调控。
结果：SRSF9表达升高与GBM分期和胶质瘤患者的低生存率相关。通过功能增益和功能损失策略，证明SRSF9促进GBM细胞的增殖和迁移。生物信息学分析表明，SRSF9对细胞生长途径有影响，包括细胞周期检查点和E2F靶标。机械上,SRSF9似乎与CDK1基因的启动子结合并增加其转录水平，从而促进GBM细胞增殖。
结论：这些发现揭示了SRSF9在GBM中的细胞功能，并强调了其对GBM的治疗潜力。
方法：进行生物信息学分析，以探讨SRSF9在GBM中的差异表达及其与胶质瘤患者预后的相关性。通过RT-qPCR定量GBM细胞系和患者组织中的SRSF9和CDK1表达，蛋白质印迹或免疫荧光测定。MTT法评价SRSF9在GBM细胞增殖和迁移中的作用,Transwell和集落形成测定。此外,使用ChIP-PCR和双荧光素酶测定法研究了SRSF9对CDK1的转录调控。
结果：SRSF9表达升高与GBM分期和胶质瘤患者的低生存率相关。通过功能增益和功能损失策略，证明SRSF9促进GBM细胞的增殖和迁移。生物信息学分析表明，SRSF9对细胞生长途径有影响，包括细胞周期检查点和E2F靶标。机械上,SRSF9似乎与CDK1基因的启动子结合并增加其转录水平，从而促进GBM细胞增殖。
结论：这些发现揭示了SRSF9在GBM中的细胞功能，并强调了其对GBM的治疗潜力。
