摘要
目的 研究着丝粒蛋白B(CENPB)在胶质瘤组织中的表达与患者预后的关系并分析其生物学作用。方法 基于癌症基因组图谱(TCGA)数据库,采用Wilcoxon符号秩检验比较CENPB在泛癌中的表达水平,并进一步分析了其与胶质瘤患者临床特征及预后的相关性。采用Cox回归分析和Kaplan-Meier生存曲线分析CENPB与胶质瘤生存期的相关性并绘制列线图。通过基因本体(GO)、京都基因与基因组百科全书(KEGG)数据库分析CENPB相关基因的富集途径。采用单样本基因富集分析(ssGSEA)方法,分析胶质瘤中的免疫浸润与CENPB表达的相关性。结果 同正常组织相比,CENPB基因在胶质瘤组织中高表达。CENPB在Ⅳ级胶质瘤(WHO分级)、异柠檬酸脱氢酶(IDH)野生型、无1p/19q共删除的胶质瘤组织中表达水平较高。ssGSEA显示Th2细胞浸润与胶质瘤中CENPB的表达呈正相关。结论 CENPB是神经胶质瘤的预后不良的独立危险因素,调节CENPB表达可能是治疗胶质瘤的潜在靶点。
【Objective】 To investigate the relationship between the expression of centromere protein B(CENPB) in glioma tissues and the prognosis of patients,and to analyze its biological role.【Methods】 Based on The Cancer Genome Atlas(TCGA)database,Wilcoxon signed rank test was used to compare the expression level of CENPB in pancarcinoma,and its correlation with clinical characteristics and prognosis of glioma patients was further analyzed.Cox regression analysis and Kaplan-Meier survival curve were used to analyze the correlation between CENPB and glioma survival.The enrichment pathways of CENPB-associated genes were analyzed using the Gene Ontology(GO),Kyoto Encyclopedia of Genes and Genomes(KEGG) database.Single sample gene enrichment analysis(ssGSEA) was used to analyze the correlation between immune infiltration and CENPB expression in glioma.【Results】 Compared with normal tissues,CENPB gene was highly expressed in glioma tissues.The expression level of CENPB was higher in gliomas of grade Ⅳ(WHO grade),IDH wild type,and gliomas without 1p/19q co-deletion.ssGSEA showed that Th2 cell infiltration was positively correlated with CENPB expression in glioma.【Conclusion】 CENPB is an independent risk factor for poor prognosis of glioma,and the regulation of CENPB expression may be a potential target for treatment of glioma.
作者
侯程山
向井念
付锐
HOU Chengshan;XIANG Jingnian;FU Rui(Jinzhou Medical University,Jinzhou,Liaoning 121000,China;Clinical College,Hubei University of Medicine,Shiyan,Hubei 442000,China)
出处
《中国医学工程》
2025年第2期26-32,共7页
China Medical Engineering
作者简介
通信作者:付锐,E-mail:frfrui@163.com。