Identification of the Shared Hub Gene Signatures and Biological Mechanism in Idiopathic Pulmonary Fibrosis and Inflammatory Bowel Disease
Objective To explore the potential hub molecules and pathways mediating the co-occurrence of idiopathic pulmonary fibrosis(IPF)and inflammatory bowel disease(IBD)based on bioinformatics.Methods Datasets of IPF(GSE110147)and IBD(GSE752141)were downloaded from the National Center for Biotechnology Information(NCBI)gene expression omnibus(GEO).The"limma"packages of R was used to analyze differentially expressed genes(DEGs).The biological functions of the DEGs underwent gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)analysis.Then,STRING database and Cytoscape software were used for protein-protein interaction(PPI)network,module construction and hub gene identification.Hub gene validation was performed in GSE53845 for IPF and GSE59071 for IBD.Based on the NetworkAnalyst Web platform,an interaction network for TFs-hub genes and TFs-microRNAs(miRNAs)was constructed.Results A total of 67 up-regulated genes DEGs and 23 down-regulated genes DEGs were screened out for follow-up analyses.Six important hub genes,including SPP1,COL1A1,POSTN,MMP7,COL3A1,COL6A3 were identified using CytoHubba and MCODE plugin.In the TFs-gene interaction network,SPP1 had the highest interaction rate with other TFs genes.Among the regulatory factors with the highest degree of TFs-genes interaction network,HINFP,POU2F2,YY1,FOXL1 and FOXC1 coordinately take part in the regulation of SPP1.On the other hand,among the miRNAs in the TFs-MiRNAs co-regulatory network,hsa-miR-301b,hsa-miR-301a,hsa-miR-29c,hsa-miR-29b and hsa-miR-29a showed the highest degree at three places,and all of them targeted COL6A3.Conclusion This bioinformatics study reveals the common pathogenesis of IPF and IBD,suggesting that IPF and IBD are similar,which can provide new ideas for further research.
万方数据
维普
