CCNB1 and CCNB2 involvement in the pathogenesis of psoriasis: a bioinformatics study

• Published in: Journal of international medical research Vol. 50; no. 8; p. 3000605221117138
• Main Authors: Li, An-hai, Chen, Yong-qing, Chen, Yu-qian, Song, Yun, Li, Ding
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.08.2022; Sage Publications Ltd; SAGE Publishing
• Subjects: Bioinformatics; Cell cycle; Pre-Clinical Research Report; Psoriasis; keratinocyte; psoriasis; cyclin B1; mast cell; macrophage; Cell cycle-related protein; cyclin B2
• ISSN: 0300-0605; 1473-2300; 1473-2300
• DOI: 10.1177/03000605221117138

Objective The cell cycle-related proteins cyclin B1 (CCNB1) and cyclin B2 (CCNB2) are potentially involved in the underlying mechanisms of psoriasis. The present study aimed to explore this possibility using bioinformatics approaches. Methods CCNB1 and CCNB2 protein levels were evaluated in 14 psoriasis patients and five healthy controls by enzyme-linked immunosorbent assays, and their mRNA levels were evaluated using data from four publicly available datasets (GSE53552, GSE41664, GSE14905, and GSE13355). Comparison of high- and low-expressing groups were performed to reveal CCNB1- and CCNB2-related differentially expressed genes, which were then assessed based on gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. Correlation analyses between CCNB1 and CCNB2 levels and immune infiltration, as well as typical targets of psoriasis, were also performed. Results Overall, 12 CCNB1 and CCNB2 common immune-related targets potentially involved in psoriasis were identified. These could regulate the cell cycle of through multiple pathways. In addition, CCNB1 and CCNB2 were found to potentially support the release of key molecular targets of psoriasis through the regulation of mast cell activation and macrophage polarization. Conclusions These findings suggest that CCNB1 and CCNB2 may represent valuable molecular biomarkers of psoriasis, contributing to its onset and progression.