Although several studies have attempted to investigate the etiology of and mechanism underlying psoriasis, the precise molecular mechanism remains unclear. Our study aimed to explore the molecular mechanism underlying psoriasis based on bioinformatics.
GSE30999, GSE34248, GSE41662, and GSE50790 datasets were obtained from the Gene Expression Omnibus database. The Gene Expression Omnibus profiles were integrated to obtain differentially expressed genes in R software. Then a series of analyses was performed, such as Gene Ontology annotation, Kyoto Encyclopedia of Genes and Genomes pathway analysis, protein-protein interaction network analysis, among others. The key genes were obtained by CytoHubba, and validated by real-time quantitative polymerase chain reaction.
A total of 359 differentially expressed genes were identified between 270 paired lesional and non-lesional skin groups. The common enriched pathways were nucleotide-binding and oligomerization domain-like receptor signaling pathway, and cytokine-cytokine receptor interaction. Seven key genes were identified, including
CXCL1, ISG15, CXCL10, STAT1, OASL, IFIT1,
and
IFIT3.
These key genes were validated as upregulated in the 4 datasets and M5-induced HaCaT cells.
Our study identified 7 key genes, namely
CXCL1, ISG15, CXCL10, STAT1, OASL, IFIT1,
and
IFIT3
, and 2 mostly enriched pathways (nucleotide-binding and oligomerization domain-like receptor signaling pathway, and cytokine-cytokine receptor interaction) involved in psoriatic pathogenesis. More importantly,
CXCL1, ISG15, STAT1, OASL, IFIT1, IFIT3,
and especially
CXCL10
may be potential biomarkers. Therefore, our findings may bring a new perspective to the molecular mechanism underlying psoriasis and suggest potential biomarkers.
