Objective: The purpose of this study was to explore the differentially expressed genes (DEGs) in human idiopathic pulmonary fibrosis (IPF) by bioinformatics method, and to elucidate IPF from the gene level.
Methods: Gene expression profile GSE110147 was downloaded from GEO database. Genes between patients with IPF and normal controls were analyzed using the GEO2R tool. Gene ontology (GO) and gene pathway enrichment analysis is performed in the Database for Annotation, Visualization and Integrated Discovery (DAVID). In the final, the results are analyzed synthetically.
Results: A total of 9183 differentially expressed genes were identified by the above methods, among which 4545 genes were down-regulated and 4638 genes were up-regulated. Among all the upregulated genes, matrix metallopeptidase 1 (MMP1) gene was the most significant. These DEGs played an important role in the occurrence of IPF through the MAPK (mitogen-activated protein kinase) signaling pathway. In addition, there were 55 genes enrich in PD-L1 expression and PD-1 checkpoint pathway in cancer, such as AKT1 and PIK3CA.
Conclusions: Bioinformatics analysis revealed that IPF may mediate the occurrence of lung cancer through PD-L1 expression and PD-1 checkpoint pathway, providing clues for the pathogenesis of IPF and lung cancer.