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The  Nm23  gene has been acknowledged to play a crucial role in lung cancer metastasis inhibitory cascades controlled by multiple factors. Low expression or allelic deletion of  nm23-H1  is strongly linked to widespread metastasis and poor differentiation of non-small cell lung cancer (NSCLC). In this study,  nm23-H1  was down regulated in epithelial-mesenchymal transition (EMT) and stemness enhancement under cobalt chloride (CoCl 2 )-induced hypoxia in NSCLC cells. Moreover, knocking down of  nm23-H1  by shRNA apparently promoted hypoxia induced EMT and stemness, which was entirely suppressed via over expression of  nm23-H1 . Mechanistically, the Wnt/β-catenin signaling pathway was found to participate in the  nm23-H1- mediated process. Besides, XAV939 prohibited cell EMT and stemness which could be impaired by knocking down of  nm23-H1 , while stable transfection of  nm23-H1  attenuated hypoxia phonotype induced by lithium chloride (LiCl). Generally, our experiment provided evidence that  nm23-H1  can reverse hypoxia induced EMT and stemness through the inhibition of the Wnt/β-catenin pathway, which may furnish a deeper perspective into the better treatment or prognosis for NSCLC.

Nm23-H1 inhibits hypoxia induced epithelial-mesenchymal transition and stemness in non-small cell lung cancer cells