LncRNA LINC01026 Is Overexpressed in Psoriasis and Enhances Keratinocyte Cell Cycle Progression by Regulating the Ets Homologous Factor (EHF).

Psoriasis is a chronic autoimmune skin disease characterised by a high recurrence rate and epidermal hyperproliferation. Recent studies have highlighted the pathogenic roles of long non-coding RNAs (lncRNAs) in psoriasis. However, the cellular functions and underlying mechanisms of most lncRNAs remain largely unknown. In this study, we identified functional lncRNAs associated with cell cycle regulation through integrative analysis of RNA-seq datasets from a psoriasis cohort. Interestingly, we observed significant upregulation of LINC01206 in skin biopsies from psoriatic lesions, whereas its expression was downregulated following glucocorticoid treatment. Furthermore, we constructed a lncRNA-protein-coding gene (PCG) co-expression network, which revealed that LINC01206 tends to co-express with cell cycle-related genes, such as CCNB1 and CCNE1. Using an in vitro keratinocyte model, we demonstrated that LINC01206 disrupts cell cycle progression, and its knockdown induced cell cycle arrest at the G0/G1 phase. Additional functional experiments showed that the expression of hyperproliferation-associated keratins decreased upon LINC01206 knockdown. Mechanistically, LINC01206 promotes cell cycle progression at the G0/G1 phase by modulating the activity of Ets homologous factor (EHF). Our findings suggest that LINC01206 enhances keratinocyte proliferation in psoriasis by regulating cell cycle progression, making it a potential therapeutic target for psoriasis treatment.