BackgroundThe main cause of death in patients with nonâsmall cell lung cancer (NSCLC) is the progression of cancer metastasis, which can be attributed to multiple factors, such as cancer stem cells (CSCs) and epithelialâmesenchymal transition (EMT). Long nonâcoding RNAs (lncRNAs) play important roles in the regulation of the cell cycle, cell proliferation, immune responses, and metastasis in cancers, but the potential roles and mechanisms of lincRNAs in CSCâlike properties of cancer have not yet been elucidated.MethodsHuman NSCLC cell lines (A549 and H1299), highly metastatic cell lines (L9981 and 95D), and their corresponding lowâmetastatic cell lines (NL9980 and 95C) were subject to quantitative realâtime PCR and Western blot, transwell invasion, colony formation, and wound healing assays.ResultsLincâITGB1 was greatly upregulated in CSC spheres. LincâITGB1 knockdown markedly inhibited CSC formation and the expression of stemnessâassociated genes, such as Sox2, Nanog, Octâ4, câMyc, and CD133. Depletion of lincâITGB1 expression also inhibited the in vitro invasive and migratory potential of cells, and further analysis indicated that lincâITGB1 knockdown increased the expression of the epithelial marker Eâcadherin and downregulated the mesenchymal markers vimentin and fibronectin. The EMTârelated transcription factor Snail mediated these effects of lincâITGB1 in NSCLC, and overexpression of Snail significantly reversed the inhibitory effects of lincâITGB1 depletion.ConclusionOverall, our study demonstrated that lincâITGB1 promoted NSCLC cell EMT and cancer stemness by regulating Snail expression.