Secukinumab affects the expression levels of LncRNAs MEG3 and MSX2P1 in an in vitro psoriasis model

Purpose: Psoriasis is a common chronic inflammatory skin disease characterized by recurrent, scaly plaques. IL-17 plays a central role in its pathogenesis, and Secukinumab—an anti-IL-17A monoclonal antibody—is widely used for treatment. Long non-coding RNAs (LncRNAs) regulate keratinocyte proliferation and immune responses, yet their response to IL-17 inhibition remains unclear. This study aimed to investigate the effect of Secukinumab on MEG3 and MSX2P1 lncRNA expression in a psoriasis cell culture model.Materials and methods: HaCaT cells were stimulated with lipopolysaccharide (LPS) to mimic inflammatory conditions, followed by treatment with various doses of secukinumab. Cell viability was assessed at 24, 48, and 72 hours using CCK-8, with 7.5 mg/ml determined as the LD₅₀ concentration. RNA was isolated, and gene expression levels were measured via qRT-PCR.Results: The results demonstrated an approximately 20-fold reduction in MEG3 expression and an approximately 190-fold reduction in MSX2P1 expression following secukinumab treatment compared to the control group. These findings suggest that IL-17 inhibition may influence keratinocyte function through the modulation of LncRNAs associated with proliferation and inflammation.Conclusion: Secukinumab appears to alter the expression patterns of key LncRNAs in keratinocytes. Further investigation is warranted to clarify the downstream molecular pathways involved and their relevance in the clinical management of psoriasis.