Interleukin-17 Regulates Keratinocyte Proliferation in Psoriasis Through the MALAT1/miR-125b/BRD4 Axis

Abstract

This study investigated the role of LncRNA MALAT1 in psoriasis development. Serum from psoriasis patients and healthy subjects was collected, and IL-17 levels were measured. HaCaT cells were exposed to IL-17 and transfected with shMALAT1 or treated with Secukinumab. Cell viability, proliferation, and cell cycle were assessed, along with the expression of key cell cycle regulators. Various LncRNAs were analyzed, and the interaction between MALAT1 and p65 was confirmed through luciferase assays and ChIP assays. Results showed that IL-17 treatment increased cell proliferation and MALAT1 expression. p65 binding to the MALAT1 promoter enhanced keratinocyte proliferation. Secukinumab mitigated IL-17-induced cell proliferation and rescued miR-125b expression, which was reduced by IL-17. IL-17 also elevated BRD4 expression, which Secukinumab attenuated. In summary, IL-17 promotes HaCaT cell proliferation by upregulating MALAT1, with p65 facilitating this process. Secukinumab effectively counteracts these effects, restoring miR-125b levels and reducing BRD4 expression. These findings provide new insights into potential treatments for psoriasis.