Exploring key genes and mechanisms associated with idiopathic pulmonary fibrosis and lung adenocarcinoma

Abstract

AbstractBackground:As the number of studies investigating idiopathic pulmonary fibrosis (IPF) and lung adenocarcinoma (LUAD) continues to grow, increasing evidence supports a strong correlation between these two diseases. However, the underlying common pathophysiological mechanisms remain unclear.Objective：The objective of this study is to further elucidate potential key genes and pathological mechanisms associated with IPF and LUAD.Methods:We searched and downloaded the gene expression datasets for IPF patients and their corresponding normal tissue (GSE53845), as well as the datasets for LUAD patients and normal tissue (GSE176348) from the Gene Expression Omnibus (GEO) database. Using these datasets, we identified differentially expressed genes (DEGs) and common genes, which were subjected to gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. To further elucidate the underlying mechanisms of IPF and LUAD, we constructed a protein-protein interaction (PPI) network and identified transcription factors (TFs) that may regulate key genes.Results:Ninety-three common genes were identified in both the IPF and LUAD datasets with a significance level of P<0.05. Enrichment analysis revealed 936 GO terms and 13 KEGG pathways. Using cytoHubba and van plots, we selected the top thirteen key genes, including COL1A1, COL3A1, TIMP3, IGF1, CTHRC1, SULF1, MMP12, WNT3A, CCL5, GREM1, CCL19, HPGD, and AKR1C3, and further analysis of these genes was performed. GO analysis revealed significant enrichment in the regulation of animal organ morphogenesis, extracellular matrix organization, and extracellular structural organization. The KEGG pathway enrichment analysis showed that proteoglycans were significantly enriched in cancer, ovarian steroidogenesis, and arachidonic acid metabolism. Furthermore, we identified six TFs that may regulate the expression of these key genes.Conclusions:Our findings suggest that specific key genes and shared mechanisms play a role in the development and progression of both IPF and LUAD. These key genes and mechanisms may represent potential targets for therapeutic intervention and provide novel insights into the underlying pathophysiology of these diseases.