Abstract:Objective To explore the effect of long non-coding RNA nuclear enriched transcriptome 1 (lncRNA NEAT1) on the migration and invasion of laryngeal squamous cell carcinoma (LSCC) cells, and further explore the role of miR-429/zinc finger E-box binding homeobox 1 (ZEB1) axis in this process.Methods Lentivirus transfection established LSCC cells with stable knockdown lncRNA NEAT1, and lncRNA NEAT1 expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR) to verify transfection efficiency. Cell migration and invasion ability were detected by transwell assay. The expressions of epithelial-mesenchymal transition (EMT) related proteins N-cadherin, Vimentin, Slug and Snail were detected by Western blot. The potential binding sites between miR-429 and lncRNA NEAT1 and ZEB1 mRNA were analyzed by bioinformatics, and the binding of miR-429 to lncRNA NEAT1 and miR-429 to ZEB1 mRNA were verified by dual luciferase reporter gene assay. LSCC cells with knockdown lncRNA NEAT1 were transfected with miR-429 inhibitors, and ZEB1 expression was detected by Western blot. The effect of knockdown ZEB1 on LSCC cell migration, invasion and EMT of miR-429 knockdown lncRNA NEAT1 was further examined.Results Knocking down lncRNA NEAT1 reduced lncRNA NEAT1 expression in LSCC cells, inhibited cell migration and invasion, and down-regulated the expression of N-cadherin, Vimentin, Slug, and Snail. There were potential binding sites between miR-429 and lncRNA NEAT1 and ZEB1 mRNA, and miR-429 bound to lncRNA NEAT1 and miR-429 to ZEB1 mRNA. Inhibition of 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 the mechanism may be related to the upregulation of ZEB1 expression by sponging miR-429 and promoting EMT in LSCC cells.