lincROR influences the stemness and crizotinib resistance in EML–ALK<sup>+</sup> non-small-cell lung cancer cells

Abstract

We found that lincROR expression was significantly inhibited because of the increased concentration of crizotinib in EML4-ALK⁺ NSCLC cells. Furthermore, lincROR overexpression increased cell viability of EML4-ALK⁺ NSCLC cells, which was impaired by crizotinib. Conjointly, these results suggested the important role of lincROR in EML-ALK⁺ NSCLC. lincROR may serve as a potential therapeutic target to overcome chemotherapy resistance in EML-ALK⁺ NSCLC.