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鉴定与幽门螺杆菌感染胃细胞相关的枢纽基因和信号通路。

Identification of hub genes and signaling pathways related to gastric cells infected by Helicobacter pylori.

机构信息

Department of Clinical Laboratory Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510150, China; Department of Clinical Medicine, The Third Clinical School of Guangzhou Medical University, Guangzhou, 511436, China.

Nanshan School, Guangzhou Medical University, Jingxiu Road, Panyu District, Guangzhou, 511436, China.

出版信息

Microb Pathog. 2021 Jul;156:104932. doi: 10.1016/j.micpath.2021.104932. Epub 2021 May 5.

Abstract

BACKGROUND

Helicobacter pylori is a pathogen involved in several gastroduodenal diseases, whose infection mechanisms have not been completely confirmed. To study the specific mechanism of gastropathy caused by H. pylori, we analyzed the gene microarray of gastric mucosa and gastric cells infected by H. pylori through bioinformatics analysis.

METHODS

We downloaded GSE60427 and GSE74492 from the Gene Expression Omnibus (GEO) database, screened differentially expressed genes (DEGs), and identified the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) through R software. The Search Tool for the Retrieval of Interacting Genes (STRING) was applied to establish a protein-protein interaction (PPI) network and Cytoscape was used to identify the top seven hub genes. Besides, we also constructed the gene-microRNA(gene-miRNA) interaction through the miRTarBase v8.0 database by using the NetworkAnalyst tool.

RESULTS

One hundred and fifteen DEGs were screened out, with 54 genes up-regulated and 61 genes down-regulated, among which seven hub genes, including "IGF1R," "APOE," "IRS1," "ATF3," "LCN2," "IL2RG," and "PI3," were considered as the main regulatory proteins in gastric cells when infected by H. pylori.

CONCLUSION

In this study, hub genes and related signal enrichment pathways of gastropathy infected by H. pylori were analyzed through bioinformatics analysis based on the GSE60427 and GSE74492 datasets.

摘要

背景

幽门螺杆菌是一种参与多种胃十二指肠疾病的病原体,其感染机制尚未完全确定。为了研究幽门螺杆菌引起的胃病的具体机制,我们通过生物信息学分析,对感染幽门螺杆菌的胃黏膜和胃细胞的基因芯片进行了分析。

方法

我们从基因表达综合数据库(GEO)中下载了 GSE60427 和 GSE74492,筛选差异表达基因(DEGs),并通过 R 软件识别基因本体论(GO)和京都基因与基因组百科全书(KEGG)。应用搜索工具检索基因相互作用(STRING)构建蛋白质-蛋白质相互作用(PPI)网络,并使用 Cytoscape 识别前 7 个枢纽基因。此外,我们还通过 miRTarBase v8.0 数据库,利用 NetworkAnalyst 工具构建了基因-miRNA(gene-miRNA)相互作用。

结果

筛选出 115 个差异表达基因,其中 54 个基因上调,61 个基因下调,其中 7 个枢纽基因,包括“IGF1R”、“APOE”、“IRS1”、“ATF3”、“LCN2”、“IL2RG”和“PI3”,被认为是感染幽门螺杆菌时胃细胞的主要调节蛋白。

结论

本研究基于 GSE60427 和 GSE74492 数据集,通过生物信息学分析,分析了幽门螺杆菌感染性胃病的枢纽基因及相关信号富集途径。

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