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Background  Recent studies have revealed that dysregulated expression of long non-coding RNA nicotinamide nucleotide transhydrogenase antisense RNA 1 (lncRNA NNT-AS1) is associated with cell tumorigenicity in non-small cell lung cancer. However, the exact molecular mechanisms of NNT-AS1 in lung squamous cell carcinoma (LUSC) remain largely unknown.    Methods  The expression of NNT-AS1, microRNA (miR)-22 and Forkhead box protein M1 (FOXM1) was measured using quantitative real-time polymerase chain reaction or western blot, respectively. The interaction between miR-22 and NNT-AS1 or FOXM1 was confirmed using a dual-luciferase reporter assay and RNA immunoprecipitation assay. Cell migration and invasion abilities were measured by Transwell assay. Flow cytometry was used to detect apoptotic cells.    Results  NNT-AS1 and FOXM1 were up-regulated but miR-22 was down-regulated in LUSC tissues and cell lines. NNT-AS1 was a sponge of miR-22, and NNT-AS1 deletion suppressed the migration and invasion but induced apoptosis in LUSC cells. FOXM1 was a target of miR-22, and overexpression of miR-22 inhibited cell carcinogenesis in LUSC by targeting FOXM1. Additionally, NNT-AS1 could directly regulate FOXM1 expression by binding to miR-22 in LUSC cells.    Conclusion  LncRNA NNT-AS1 contributes to cell carcinogenesis in LUSC by regulating the miR-22/FOXM1 axis, providing a novel insight into the pathogenesis of LUSC and a new potential therapeutic target for LUSC treatment.

LncRNA NNT-AS1 promotes lung squamous cell carcinoma progression by regulating the miR-22/FOXM1 axis