摘要目的:探讨CXC基序趋化因子10（CXCL10）在脑胶质瘤中的表达及其对脑胶质瘤发生、发展与预后的影响。方法:分别利用生物信息学中国脑胶质瘤基因组图谱（CGGA）， 癌症基因组图谱（TCGA）、MetaScape、TIMER等数据库分析CXCL10在胶质瘤中的表达水平、对患者的预后意义、GO功能注释、KEGG通路富集及胶质瘤纯度的相关性。进一步收集2019年3至11月在广西医科大学第二附属医院诊断胶质瘤的患者34例临床胶质瘤组织标本，应用Western 印迹和免疫组化验证其相关性。结果:CGGA和TCGA数据库分析显示，CXCL10在胶质瘤中随着世界卫生组织（WHO）分级的增高表达水平升高（CGGA： F=86.69， P<0.01；TCGA： F=68.17， P<0.01）。CXCL10高表达的患者总生存率明显下降（ χ 2 = 148.1， P<0.05）。在接受放疗或化疗的Ⅳ级胶质瘤患者中，CXCL10低表达患者总生存率明显优于高表达患者（放疗组： χ 2 = 6.714 ，P<0.05；化疗组： χ 2 = 5.618 ，P<0.05）。GO和KEGG分析表明与CXCL10共表达的基因主要富集在细胞因子介导的信号通路、调节适应性免疫反应及炎症反应等生物学过程中。TIMER数据库分析显示CXCL10与胶质瘤肿瘤细胞纯度负相关［低级别胶质瘤（LGG）： r=-0.129；胶质母细胞瘤（GBM）： r=-0.165； P<0.05］。同时，临床样本分析也显示CXCL10在胶质瘤中表达升高并随级别升高而表达升高（均 P<0.05）。 结论:CXCL10在胶质瘤中表达升高，且随恶性程度的增高而升高，胶质瘤组织中CXCL10高表达与患者不良预后相关。

abstractsObjective:To analyze the expression of CXC chemokine ligand 10 (CXCL10) in glioma and its clinical significance through bioinformatics.Methods:The expression level of CXCL10 in glioma, and its prognostic significance, gene ontology (GO) function annotation, Kyoto Encyclopedia of Genes and Genome (KEGG) pathway enrichment and the correlation of tumor cell purity were analyzed in TCGA, CGGA, MetaScape, TIMER databases. In addition, 34 clinical glioma tissues were collected for Western Blot and immunohistochemistry to further verify the correlation between CXCL10 and glioma.Results:CGGA and TCGA database analysis showed that with the increase of WHO grade, the expression of CXCL10 in gliomas increased ( P<0.01). The overall survival rate of patients with high CXCL10 expression was significantly lower than that of patients with low expression ( χ 2 = 148.1, P<0.05). Among patients with grade Ⅳ glioblastoma who received radiotherapy or chemotherapy, the patients with low CXCL10 expression were associated with good survival ( χ 2 = 6.714 ,P<0.05; χ 2 = 5.618 ,P<0.05). Moreover, GO and KEGG analysis showed that genes co-expressed with CXCL10 were mainly enriched in the biological processes such as cytokine-mediated signaling pathways, regulating adaptive immune responses and inflammatory responses. Furthermore, TIMER database analysis showed that CXCL10 was negatively correlated with the purity of glioma cells (LGG: r=-0.129;GBM: r=-0.165; P<0.05). Similarly, clinical sample analysis also showed that the expression level of CXCL10 increased in glioma, and it increased with the grade of glioma (all P<0.05). Conclusion:The expression of CXCL10 is up-regulated in glioma as well as it increased with the malignant degree of glioma. At the same time, the high expression of CXCL10 in glioma is closely related to the poor prognosis of patients.