HOTAIR induces EGFR-TKIs resistance in non-small cell lung cancer through epithelial-mesenchymal transition.

•Down-regulation of HOTAIR was associated with EGFR-TKIs resistance.•HOTAIR may enhance activation of apoptosis and EMT.•HOTAIR overexpression restored gefitinib sensitivity in EGFR-TKI resistant cell lines.•HOTAIR expression was associated with primary and acquired resistance to EGFR-TKIs.•HOTAIR might be able to act as a biomarker to predict the EGFR-TKIs resistance.