PDF(Pubmed)
Abstract：
BACKGROUND: Immune cell infiltration plays a critical role in regulating peptic ulcer disease (PUD) and gastrointestinal cancer (GC). However, regulators of the cell signaling hubs remain unclear.
OBJECTIVE: This study characterizes genes that are differentially expressed in PUD and GC tissue samples. Bioinformatics is used to define the immune-associated hub genes associated with the malignant transfer process of PUD to GC.
METHODS: Total expression data from PUD and early-stage GC tissue samples were obtained from GEO and TCGA. Differentially expressed genes were assessed and immunological enrichment analysis was performed. Protein-protein interaction (PPI) and Cytoscape analysis were used together to identify the hub genes. CIBERSORT and COX analysis were used to analyze the differentially infiltrated immune cell landscapes and determine HR scores of the hub genes.
RESULTS: Expression data identified 437 DEGs as common to both GC and PUD tissue. Of these, 49 immune-related DEGs were grouped by function, and seven hub genes were identified by PPI analysis. The NRP2 and SEMA3D genes were then selected for survival analysis. SEMA3D had a higher hazard ratio than NRP2 and was defined as the hub for PUD carcinogenesis.
CONCLUSIONS: SEMA3D was characterized as the hub gene for PUD carcinogenesis.
OBJECTIVE: This study characterizes genes that are differentially expressed in PUD and GC tissue samples. Bioinformatics is used to define the immune-associated hub genes associated with the malignant transfer process of PUD to GC.
METHODS: Total expression data from PUD and early-stage GC tissue samples were obtained from GEO and TCGA. Differentially expressed genes were assessed and immunological enrichment analysis was performed. Protein-protein interaction (PPI) and Cytoscape analysis were used together to identify the hub genes. CIBERSORT and COX analysis were used to analyze the differentially infiltrated immune cell landscapes and determine HR scores of the hub genes.
RESULTS: Expression data identified 437 DEGs as common to both GC and PUD tissue. Of these, 49 immune-related DEGs were grouped by function, and seven hub genes were identified by PPI analysis. The NRP2 and SEMA3D genes were then selected for survival analysis. SEMA3D had a higher hazard ratio than NRP2 and was defined as the hub for PUD carcinogenesis.
CONCLUSIONS: SEMA3D was characterized as the hub gene for PUD carcinogenesis.
摘要：
背景：免疫细胞浸润在调节消化性溃疡（PUD）和胃肠道癌（GC）中起关键作用。然而,细胞信号枢纽的监管机构仍不清楚。
目的：本研究表征了PUD和GC组织样品中差异表达的基因。生物信息学用于定义与PUD向GC的恶性转移过程相关的免疫相关hub基因。
方法：从GEO和TCGA获得PUD和早期GC组织样品的总表达数据。评估差异表达的基因并进行免疫富集分析。蛋白-蛋白相互作用(PPI)和Cytoscape分析一起用于鉴定hub基因。CIBERSORT和COX分析用于分析差异浸润的免疫细胞景观并确定枢纽基因的HR得分。
结果：表达数据将437个DEG鉴定为GC和PUD组织共有。其中,49个免疫相关的DEGs按功能分组，通过PPI分析鉴定出7个hub基因。然后选择NRP2和SEMA3D基因用于存活分析。SEMA3D的危险比高于NRP2，被定义为PUD致癌作用的中心。
结论：SEMA3D是PUD癌变的中心基因。
目的：本研究表征了PUD和GC组织样品中差异表达的基因。生物信息学用于定义与PUD向GC的恶性转移过程相关的免疫相关hub基因。
方法：从GEO和TCGA获得PUD和早期GC组织样品的总表达数据。评估差异表达的基因并进行免疫富集分析。蛋白-蛋白相互作用(PPI)和Cytoscape分析一起用于鉴定hub基因。CIBERSORT和COX分析用于分析差异浸润的免疫细胞景观并确定枢纽基因的HR得分。
结果：表达数据将437个DEG鉴定为GC和PUD组织共有。其中,49个免疫相关的DEGs按功能分组，通过PPI分析鉴定出7个hub基因。然后选择NRP2和SEMA3D基因用于存活分析。SEMA3D的危险比高于NRP2，被定义为PUD致癌作用的中心。
结论：SEMA3D是PUD癌变的中心基因。
