CXCL10 and its related key genes as potential biomarkers for psoriasis

Abstract

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.

Bioinformatics analysis to reveal the potential comorbidity mechanism in psoriasis and nonalcoholic steatohepatitis

“…As members of IFIT (IFN‐γ stimulated genes) family, IFIT1 and IFIT3 may act as a regulator of anti‐inflammatory and immune responses 29,30 . In some researches, IFIT1 was identified low expression when interventions were used to suppress nonalcoholic hepatitis, 29,31 and the expression of IFIT1 and IFIT3 was validated as upregulated in psoriasis, 21,32–34 which was consistent with the high expression in both psoriasis and NASH we found. OAS1 is a member of OASs (2′−5′‐oligoadenylate synthetases) family, which also contains OAS2, OAS3, and OASL, being IFN‐induced enzymes with multiple antiviral activities.…”

Weighted Gene Co-Expression Network Analysis of Oxymatrine in Psoriasis Treatment

“…34 T cells also produce large amounts of other types of cytokines that interact with each other, resulting in skin thickening and inflammatory cell infiltration. 35,36 Meanwhile, using RNA sequencing analysis, Tervaniemi et al identified NLR signal transduction in immune-related pathways of psoriasis, with NOD2 upregulated in psoriatic epidermis. 33 Indeed, the epidermal cell cycle is altered in patients with psoriasis compared with that in normal subjects.…”

Bioinformatics analysis of the shared pathogenesis of psoriasis and Crohn's disease

“…CXCL1 and CXCL10 genes are members of the CXC chemokine gene family, CXCL10 gene is located on human chromosome 4 along with CXCL1 11,12 . Interestingly, CXCL1 and CXCL10 genes were also identi ed as hub genes in another bioinformatics analysis of psoriasis and were validated by RT-qPCR in HaCaT cells, showing high expression 13 . CXCL1 gene is ampli ed in various in ammatory and cancer diseases including Crohn's disease 14,15 .…”