ITGA2在人脑胶质瘤组织中的表达及其临床意义

目的观察整合素alpha-2（ITGA2）在人脑胶质瘤组织与正常脑组织中的表达差异，分析其表达水平与胶质瘤病理分级、预后及肿瘤免疫微环境的关系。方法采用公共数据库分析ITGA2在不同级别的胶质瘤组织中mRNA表达变化及其与患者预后关系，同时应用免疫印迹检测ITGA2蛋白水平在不同级别胶质瘤组织中的表达水平。采用Kaplan-Meier、单因素和多因素Cox分析和受试者工作特征曲线评价ITGA2表达水平对预后的影响。采用GO、KEGG富集分析方法筛选ITGA2调控的功能或通路。利用ESTIMATE算法、Cibersort算法和TIMER数据库，探讨ITGA2表达水平与免疫微环境的关系。结果在公共胶质瘤数据库和本研究收集的胶质瘤标本中均显示ITGA2 mRNA和蛋白水平在WHO Ⅳ级胶质瘤中表达显著升高。ITGA2高表达组的胶质瘤患者总生存期显著低于ITGA2低表达组。ITGA2表达水平与免疫评分、免疫检查点和免疫细胞浸润有关。结论ITGA2在胶质瘤中过表达，与患者的预后和肿瘤免疫有关，提示ITGA2可能是胶质瘤免疫治疗的新靶点。

ObjectiveTo observe the different expression of Integrin alpha 2(ITGA2) in human glioma tissues and normal brain tissues, and to analyze the connection between its expression level and pathological grades, prognosis and tumor immune microenvironment of glioma. MethodsPublic databases were used to analyze the mRNA expression changes of ITGA2 in glioma tissues with different grades and its relationship with clinical prognosis. Western blot was used to detect ITGA2 protein levels in glioma tissues of different grades. Then, Kaplan-Meier survival analysis, univariate and multivariate Cox analysis, and receiver operating characteristic curve analysis were used to evaluate the effect of ITGA2 on prognosis. GO and KEGG enrichment analysis were used to screen the function or pathway regulated by ITGA2. Moreover, the ESTIMATE algorithm, Cibersort algorithm, and TIMER database were used to explore the relationship between ITGA2 expression level and immune microenvironment. ResultsIn the public glioma datasets and the glioma tissues collected by this study, the ITGA2 mRNA and protein levels increased with the increase in pathological grades, and its expression was significantly up-regulated in WHO Ⅳ grade glioma tissues. The overall survival was significantly shortened in patients with high ITGA2 expression than that in the ITGA2 low expression group. In addition, the expression level of ITGA2 was related to immune score, immune checkpoint and immune cell infiltration. ConclusionThe overexpression of ITGA2 in glioma is related to the prognosis of patients and tumor immunity, suggesting that ITGA2 may be a new target for glioma immunotherapy.