Abstract <p>Long non-coding RNA (lncRNA) SNHG1 has been reported to play an oncogenic role in various cancers. However, its specific role and underlying mechanisms in osteosarcoma (OS) remain unclear. This study aimed to investigate the expression, function, and potential mechanisms of lncRNA SNHG1 in OS. Human OS cell lines (MG-63, U2OS, Saos-2) and the normal human osteoblast cell line (hFOB 1.19) were cultured. Small interfering RNA targeting SNHG1 (si-SNHG1), miR-182-5p mimics, miR-182-5p inhibitor, and corresponding negative controls were transfected into cells. Cell proliferation was assessed using the CCK-8 assay, while cell migration and invasion were evaluated via the Transwell assay. The dual-luciferase reporter assay was employed to verify the targeting relationships between SNHG1 and miR-182-5p, as well as between miR-182-5p and KIF18A. qRT-PCR demonstrated that SNHG1 was significantly upregulated in OS cell lines, whereas miR-182-5p was downregulated, showing a negative correlation between their expression levels. Functional experiments revealed that silencing SNHG1 or overexpressing miR-182-5p significantly inhibited the proliferation, migration, and invasion of OS cells. The dual-luciferase reporter assay confirmed that SNHG1 directly targeted miR-182-5p, and miR-182-5p targeted KIF18A. Western blot analysis indicated that SNHG1 regulated KIF18A protein expression by modulating miR-182-5p. LncRNA SNHG1 is highly expressed in OS cells and promotes their proliferation, migration, and invasion. Its mechanism of action may involve functioning as a competitive endogenous RNA (ceRNA) to sequester miR-182-5p, thereby relieving the suppressive effect of miR-182-5p on KIF18A and promoting KIF18A expression. Thus, SNHG1 facilitates OS progression via the miR-182-5p/KIF18A axis.</p>