增龄相关慢性萎缩性胃炎的生物信息学分析
A bioinformatics analysis of age-related chronic atrophic gastritis
邵琳琳 1秦达 1郭水龙2
作者信息
- 1. 首都医科大学附属北京友谊医院消化内科 北京 100050
- 2. 首都医科大学附属北京友谊医院科技处 北京 100050
- 折叠
摘要
目的 应用生物信息学方法,探究增龄相关慢性萎缩性胃炎的潜在基因及生物调控途径.方法 运用4大基因信息数据库,筛选调控增龄、萎缩和胃炎的基因,使用DAVID在线工具,进行基因功能注释及通路分析,利用STRING数据库,构建蛋白质相互作用网络(PPI),寻找核心基因及调控模块,并预测相关的miRNAs.结果 共筛选出860个共同靶点基因,分子功能集中在信号受体激活,细胞组分定位主要在细胞膜外侧,miRNA信号通路、细胞因子-细胞因子受体相互作用、动脉粥样硬化等有较多的靶点基因富集.PPI分析显示,白细胞介素(IL)-6、IL-10和白血病抑制因子(LIF)是核心基因.miRNAs预测显示:miR-223-3p、miR-106a-5p及miR-98-5p可能参与增龄相关慢性萎缩性胃炎的发生、发展.结论 IL-6、IL-10和LIF基因及miR-223-3p信号通路可能是治疗增龄相关慢性萎缩性胃炎的靶点.
Abstract
Objective To explore the potential target genes and biological regulation pathways of age-related chronic atrophic gastritis by using bioinformatics methods.Methods The genes regulating aging,atrophic and gastritis were screened from the four major gene information da-tabases.DAVID online tool was used for gene function annotation and pathway analysis.Using the STRING database,a protein-protein interac-tion network(PPI)was constructed to search for core genes and regulatory modules,and to predict related miRNAs.Results A total of 860 com-mon target genes were screened.Molecular functions predominantly concentrated in signal receptor activation and cellular component mainly local-ized outside of the cell membrane.There was significant enrichment of target genes in pathways such as the miRNA signaling pathway,cytokine-cytokine receptor interaction,and atherosclerosis.PPI analysis revealed interleukin(IL)-6,IL-10,and leukemia inhibitory factor(LIF)were the core genes.miRNA predictions suggest that miR-223-3p,miR-106a-5p,and miR-98-5p may be involved in the occurrence and de-velopment of age-related atrophic gastritis.Conclusion IL-6,IL-10,and LIF genes,along with the miR-223-3p signaling pathway may be the potential target of treatment of age-related atrophic gastritis.
关键词
增龄相关慢性萎缩性胃炎/生物信息学/潜在基因/调控途径Key words
Age-related chronic atrophic gastritis/Bioinformatics/Potential target genes/Regulatory pathway引用本文复制引用
基金项目
国家自然科学基金青年项目(81902472)
出版年
2024