Abstract： Objective： To investigate the effect and mechanism of butein on glycolysis， apoptosis， migration and invasion of oral squamous cell carcinoma(HSC-3) cells. Methods：HSC-3 cells were treated with different concentrations of butein， and cell apoptosis， migration and invasion were detected by flow cytometry and Transwell assay. The kit detects glucose consumption and lactic acid production. The expressions of long- chain noncoding RNA(lncRNA) STXBP5 antisense RNA1(STXBP5- AS1) and miR- 892a were detected by real- time fluorescence quantitative PCR(RT- qPCR). The regulatory relationship between STXBP5-AS1 and miR-892a was analyzed and verified by double Luciferase Report experiment and RTqPCR. STXBP5- AS1 overexpression plasmid was transfected into HSC- 3 cells to detect the effects of STXBP5- AS1 overexpression on cell glycolysis，apoptosis，migration and invasion. Transfect STXBP5-AS1 small interfering RNA into HSC-3 cells，and detect the effects of inhibiting the expression of STXBP5-AS1 on glycolysis，apoptosis，migration and invasion of butein treated HSC- 3 cells. Results： After butein treatment， the glucose consumption， lactic acid production， migration and invasion of HSC-3 cells decreased significantly，the apoptosis rate increased significantly，the expression of STXBP5- AS1 increased significantly，and the expression of miR-892a decreased significantly(P＜0.05). miR-892a is the target gene of STXBP5- AS1. After overexpression of STXBP5- AS1，glucose consumption，lactate production，migration and invasion of HSC-3 cells decreased significantly，the apoptosis rate increased significantly，and the expression of miR-892a decreased significantly(P＜0.05). Inhibition of STXBP5- AS1 expression could reduce the effects of butein treatment on glycolysis， apoptosis， migration and invasion of HSC- 3 cells(P＜0.05). Conclusion： Butein can inhibit the migration， invasion， glycolysis and metabolism of HSC- 3 cells and promote cell apoptosis. Its mechanism may be related to the regulation of lncRNA STXBP5-AS1/miR-892a axis.