Background. Ulcerative colitis (UC) is a complicated disease caused by the interaction between genetic and environmental factors that affect mucosal homeostasis and triggers inappropriate immune response. The purpose of the study was to identify significant biomarkers with potential therapeutic targets and the underlying mechanisms. Methods. The gene expression profiles of GSE48958, GSE73661, and GSE59071 are from the GEO database. Differentially expressed genes (DEGs) were screened by the GEO2R tool. Next, the Database for Annotation, Visualization and Integrated Discovery (DAVID) was applied to analyze gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Then, protein-protein interaction (PPI) was visualized by Cytoscape with Search Tool for the Retrieval of Interacting Genes (STRING). Results. There were a total of 128 common DEGs genes, including 86 upregulated genes enriched in extracellular space, regulation of inflammatory response, chemokine-mediated signaling pathway, response to lipopolysaccharide, and cell proliferation, while 42 downregulated genes enriched in the integral component of the membrane, the integral component of the plasma membrane, apical plasma membrane, symporter activity, and chloride channel activity. The KEGG pathway analysis results demonstrated that DEGs were particularly enriched in cytokine-cytokine receptor interaction, TNF signaling pathway, chemokine signaling pathway, pertussis, and rheumatoid arthritis. 18 central modules of the PPI networks were selected with Cytotype MCODE. Furthermore, 18 genes were found to significantly enrich in the extracellular space, inflammatory response, chemokine-mediated signaling pathway, TNF signaling pathway, regulation of cell proliferation, and immune response via reanalysis of DAVID. Conclusion. The study identified DEGs, key target genes, functional pathways, and pathway analysis of UC, which may provide potential molecular targets and diagnostic biomarkers for UC.

中文翻译：

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通过生物信息学分析鉴定溃疡性结肠炎的差异肠粘膜转录组生物标志物

背景。溃疡性结肠炎 (UC) 是一种复杂的疾病，由遗传和环境因素相互作用引起，影响黏膜稳态并引发不适当的免疫反应。该研究的目的是确定具有潜在治疗靶点和潜在机制的重要生物标志物。方法. GSE48958、GSE73661 和 GSE59071 的基因表达谱来自 GEO 数据库。通过 GEO2R 工具筛选差异表达基因 (DEG)。接下来，应用注释、可视化和集成发现数据库 (DAVID) 来分析基因本体 (GO) 和京都基因和基因组百科全书 (KEGG) 通路。然后，使用用于检索相互作用基因的搜索工具 (STRING) 由 Cytoscape 可视化蛋白质-蛋白质相互作用 (PPI)。结果. 共有128个常见的DEGs基因，其中86个上调基因富集于细胞外空间、炎症反应调节、趋化因子介导的信号通路、脂多糖反应和细胞增殖，而42个下调基因富集于细胞膜的组成部分，质膜的组成部分，顶端质膜，同向转运体活性和氯离子通道活性。KEGG通路分析结果表明，DEGs特别富含细胞因子-细胞因子受体相互作用、TNF信号通路、趋化因子信号通路、百日咳和类风湿关节炎。使用 Cytotype MCODE 选择了 PPI 网络的 18 个中心模块。此外，发现 18 个基因在细胞外空间、炎症反应、结论。该研究确定了UC的DEGs、关键靶基因、功能通路和通路分析，可能为UC提供潜在的分子靶点和诊断生物标志物。