基于生物信息学的慢性胃炎-胃癌“炎癌转变”关键基因与通路研究

Identification of Genesand Pathways in Transformation from Chronic Gastritis to Gastric Cancer Using Bioinformatics Analysis

目的使用生物信息学方法,从分子水平揭示慢性胃炎-胃癌"炎癌转变"关键基因与通路,以揭示胃癌的发病机制。方法从GEO数据库中下载GSE55696基因芯片数据,利用R语言Limma包筛选出慢性胃炎→异型增生→胃癌间共同表达的差异基因,进行GO和KEGG通路富集,并构建蛋白质-蛋白质相互作用网络,以明确其关键基因。结果慢性胃炎-胃癌过程的共同差异基因有57个,均为上调基因。GO和KEGG分析显示,差异表达基因分别富集于16条生物过程条目和4条信号通路。PPI网络模块鉴定出8个关键蛋白,分别为IL8、FPR1、FCGR3A、S100A8、S100A9、CXCR2、MMP9、CCL3。结论本研究所鉴定的差异表达基因和通路可促进对慢性胃炎-胃癌"炎癌转变"机制的理解,并且可能成为胃癌诊断和预防的分子生物标记物,并为中医药改善慢性胃炎,阻断"炎癌转变"提供新的思路。

Objective This work aimed to illuminate the potential key genes and pathways in the transformation from chronic gastritis to gastric cancer based on bioinformatics analysis.Methods The differentially expressed genes(DEGs)were investigated using the GSE55696 microarray data from the Gene Expression Omnibus(GEO)database.DEGs were identified by an empirical Bayes method based on the Limma R package.And then,KEGG and GO enrichment analyses of DEGs were performed,followed by a protein-protein interaction network construction.And the key genes involving in the pathogenesis were obtained.Results A total of 57 key genes were obtained,all of which were up-regulated.Through the GO and KEGG pathway enrichment,the DEGs were enriched in 16 GO terms and 4 pathways.A PPI network of DEGs was constructed,and 8 genes including IL8,FPR1,FCGR3 A,S100 A8,S100 A9,CXCR2,MMP9 and CCL3 were selected as hub genes owing to high degrees in the network.Conclusion The key genes and pathways identified in this study can promote the understanding of the mechanism in the transformation from chronic gastritis to gastric cancer,and may become molecular biomarkers for the diagnosis and prevention of gastric cancer,which provide a new method for traditional Chinese medicine to block the transformation from inflammatory to carcinoma.