<p>Psoriasis is an immune-mediated skin disease whose pathogenesis involves aberrant keratinocyte proliferation and immune dysregulation. The long non-coding RNA PVT1 has been implicated in various diseases, but its specific role in psoriasis remains unclear. The objectives of this study were to investigate the expression and functional role of PVT1 in psoriasis, and to explore its potential interaction with miR-485-5p. The PVT1 expression level in blood serum of psoriasis patients and healthy controls were detected by RT-qPCR. A psoriasis model in vitro was established by stimulating HaCaT keratinocytes with the M5. PVT1 was knocked down by transfecting siRNA. Functional assays included CCK-8 for proliferation, ELISA for inflammatory factors/chemokines, and dual-luciferase reporter assay for target verification. PVT1 was significantly upregulated in psoriasis patients, with expression levels positively correlating with psoriasis severity. In M5-stimulated HaCaT cells, PVT1 knockdown suppressed keratinocyte hyperproliferation and reduced the secretion of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and chemokines (CXCL1, CXCL8, CCL20). Mechanistically, PVT1 was confirmed to directly bind to and negatively regulate miR-485-5p, which was downregulated in patient samples. Rescue experiments co-transfecting si-PVT1 and miR-485-5p inhibitor partially reversed the suppressive effects of PVT1 knockdown. PVT1 was overexpressed in psoriasis and promoted disease progression by enhancing keratinocyte proliferation, inflammatory responses and chemokine, likely through the targeted downregulation of miR-485-5p. These findings suggested the PVT1/miR-485-5p axis may be a promising target for psoriasis therapy.</p>