SPRR2B knockdown inhibits proliferation and inflammatory response in M5-treated human HaCaT keratinocytes
Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and excessive immune activation, for which curative therapies remain limited. This study aimed to investigate the role of small proline-rich protein 2B (SPRR2B) in psoriasis pathogenesis. In this study, gene Expression Omnibus (GEO) dataset GSE13355 was analyzed using R Language. Cell proliferation, gene and protein expression were measured with CCK8, RT-qPCR and immunofluorescence staining, respectively. Bioinformatics analysis of the GSE13355 dataset revealed that SPRR2B was significantly overexpressed in psoriatic lesions and was positively correlated with immune cell infiltration and multiple inflammatory pathways. In an M5-induced HaCaT keratinocyte psoriatic model, SPRR2B knockdown markedly suppressed cell proliferation and promoted apoptosis via regulation of the MDM2/p53/CDKN1A axis. Furthermore, SPRR2B knockdown reduced the secretion of IL-6, IFN-y, TNF-a, and IL-1p, and inhibited JAK1 phosphorylation. These findings demonstrated that SPRR2B promotes keratinocyte proliferation and inflammatory response in psoriasis, suggesting it may serve as a promising diagnostic biomarker and therapeutic target for the disease.