Objective To explore the effect of lncRNA NEAT1 on the migration and invasion of laryngeal squamous cell carcinoma cells, and further exploring the role of miR-429/ZEB1 axis in this process. Methods Slow virus transfection established stable knockdown of lncRNA NEAT1 in laryngeal squamous cell carcinoma cells. The expression of lncRNA NEAT1 was detected by RT-qPCR to verify transfection efficiency. Cell migration and invasion ability were detected by Transwell assay, and the expression of EMT related proteins N-cadherin, Vimentin, Slug, and Snail was detected by Western blot. Analyze the potential binding sites between miR-429 and lncRNA NEAT1 and ZEB1 mRNA through bioinformatics, and validate the binding of miR-429 to lncRNA NEAT1 and miR-429 to ZEB1 mRNA through dual luciferase reporter gene experiments. Transfect LSCC cells with lncRNA NEAT1 knockdown using miR-429 inhibitor and detect ZEB1 expression by Western blot. Further examination of the impact of knocking down ZEB1 on the migration, invasion, and EMT of LSCC cells that inhibit miR-429 knockdown lncRNA NEAT1. ResultsKnocking down lncRNA NEAT1 reduces the expression of lncRNA NEAT1 in LSCC cells, inhibits cell migration and invasion, and downregulates the expression of N-cadherin, Vimentin, Slug, and Snail in cells. There are potential binding sites between miR-429 and lncRNA NEAT1 and ZEB1 mRNA, and miR-429 binds to lncRNA NEAT1 and miR-429 with ZEB1 mRNA. Inhibiting miR-429 reversed the inhibitory effect of knocking down lncRNA NEAT1 on ZEB1 expression in LSCC cells. In addition, knockdown of ZEB1 reversed the inhibitory effect of miR-429 on the migration and invasion of LSCC cells with knockdown lncRNA NEAT1, as well as the upregulation of EMT related proteins N-cadherin, Vimentin, Slug, and Snail expression. Conclusion LncRNA NEAT1 promotes migration and invasion of LSCC cells, and its mechanism may be related to the upregulation of ZEB1 expression by spongy miR-429, which promotes EMT in LSCC cells.