Aims: Gliomas are the most common malignant brain neoplasms with high recurrence and lethality rates. Recently, studies have reported that cyclin-dependent kinase 5 (CDK5) is involved in tumorigenesis. Herein, we applied bioinformatics analysis to determine the clinical value of CDK5 in patients with glioma and examined the effects of CDK5 on glioblastoma cell proliferation, apoptosis, and cell cycle in vitro./nMethods: Gene expression profiles containing clinical data of low-grade glioma (LGG) and glioblastoma cohorts were obtained from The Cancer Genome Atlas database and analyzed to determine the association between CDK5 expression and glioma clinicopathological characteristics. Kaplan-Meier survival analysis was performed for prognosis analysis. Gene set enrichment analysis (GSEA) was used to identify the biological pathways involved in differential CDK5 expression. In vitro experiments were performed to explore the effects of CDK5 on glioma cell functions./nResults: CDK5 expression was substantially higher in glioblastoma than in LGG. GSEA showed that some metabolism-related pathways were associated with the high CDK5 expression phenotype. In vitro experiments showed that CDK5 knockdown impaired cell proliferation and colony formation ability, and induced apoptosis and cell cycle arrest./nConclusion: CDK5 may act as a potential biomarker of glioma progression and a valid target for glioma therapy.

中文翻译：

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CDK5组合式抑制人胶质母细胞瘤的增殖并诱导凋亡和细胞周期阻滞

目的：神经胶质瘤是最常见的恶性脑肿瘤，具有高复发率和致死率。最近，研究报道了细胞周期蛋白依赖性激酶5（CDK5）参与肿瘤发生。在此，我们应用生物信息学分析，以确定CDK5的胶质瘤患者的临床价值和研究CDK5对胶质母细胞瘤细胞增殖，凋亡和细胞周期的影响体外./n方法：从癌症基因组图谱数据库中获得了包含低度神经胶质瘤（LGG）和胶质母细胞瘤队列临床数据的基因表达谱，并进行了分析，以确定CDK5表达与神经胶质瘤临床病理特征之间的关联。进行Kaplan-Meier生存分析以进行预后分析。基因集富集分析（GSEA）用于鉴定CDK5表达差异的生物学途径。进行了体外实验以探索CDK5对神经胶质瘤细胞功能的影响。/n结果：胶质母细胞瘤中CDK5的表达明显高于LGG。GSEA显示某些与代谢有关的途径与高CDK5表达表型有关。体外实验表明，CDK5敲低会损害细胞增殖和集落形成能力，并诱导细胞凋亡和细胞周期停滞。/n结论： CDK5可能是神经胶质瘤进展的潜在生物标志物，是神经胶质瘤治疗的有效靶标。