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Forkhead box Q1 (FoxQ1) is a member of the forkhead transcription factor family.High expression of FoxQ1 has been associated with several cancers, but its role in the development of non-small cell lung cancer (NSCLC) is not clear.In this study, we investigated the expression and relationship with clinicopathologic factors of FoxQ1 in NSCLC, meanwhile, we explored the effect of FoxQ1 up-regulated and down-regulated in vitro and in vivo, and the role of FoxQ1 in regulating epithelial-mesenchymal transition (EMT) in NSCLC, providing evidence that FoxQ 1 could be a potential therapeutic target in NSCLC.FoxQ1 mRNA and protein were up-regulated in NSCLC compared with normal tissues.High expression of FoxQ1 correlated with loss of E-cad expression, and anomalous positivity of VIM and S 100A4.High expression of FoxQ1 was independent prognostic factor in NSCLC.NSCLC cells with silenced FoxQ1 had decreased cell proliferation, migration and invasion in cell culture and delayed growth of xenograft tumors in mice compared with corresponding control cells.The NSCLC cells downregulated for FoxQ1 induced the expression of apoptosis-associated proteins and reduction of anti-apoptotic protein expression.Downregulation of FoxQ1 promoted the expression of epithelial markers and decreased several mesenchymal markers in vitro and in vivo.In addition, FoxQ1 was associated with resistance to conventional chemotherapeutic agents.In contrast, FoxQ1 overexpressed elicited converse effects on these phenotypes in vitro and in vivo.Our findings define a prognostic factor for NSCLC, and the key role for FoxQ1 in regulating EMT and increasing chemosensitivityin NSCLC.