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OBJECTIVE The potential molecular mechanism underlying the disease progression of oral squamous cell carcinoma (OSCC) remains largely elusive. The purpose of the study is to figure out the role and molecular mechanism of homeobox B8 (HOXB8) in OSCC. MATERIALS AND METHODS The expression level of HOXB8 in OSCC was validated by RT-qPCR. The functions of HOXB8 in OSCC cells were identified through loss-of function assays, including CCK-8 assay, colony formation assay, transwell assay and immunofluorescence (IF). The upstream miRNA that could directly target HOXB8 was searched out through bioinformatics analysis and luciferase reporter assay. Mechanism experiments were further conducted to predict the long non-coding RNA (lncRNA) that could positively regulate HOXB8 and compete for miR-2682-5p with HOXB8. RESULTS HOXB8 was markedly upregulated in OSCC tissues and cell lines. Furthermore, cell proliferation and migration were inhibited due to the shortage of HOXB8. HOXB8 was targeted by miR-2682-5p that negatively regulated cell proliferation and migration. Small nucleolar RNA host gene 3 (SNHG3) acted as a sponge for miR-2682-5p. Inhibition of miR-2682-5p or the overexpression of HOXB8 rescued the effects of SNHG3 silencing on the proliferation and migration. CONCLUSION HOXB8 is regulated by SNHG3/miR-2682-5p axis to promote OSCC cell proliferation and migration.