Abstract
Long non‑coding RNAs (lncRNAs) have been reported to be involved in the physiological and pathological processes of tumor pathogenesis, including epithelial‑mesenchymal transition (EMT). However, epidermal growth factor receptor (EGFR)‑tyrosine kinase inhibitor (TKI) resistance is a major challenge in the treatment of advanced and recurrent EGFR‑mutant lung adenocarcinoma. An increased understanding of the underlying mechanisms would aid in the development of effective therapeutic strategies against EGFR‑TKI resistance, strategies which are urgently required for clinical therapy. In this study, long non‑coding RNA LINC00460 was identified as a novel marker of a poor response to EGFR‑TKI and prognosis. In lung cancer cells, LINC00460 promoted EGFR‑TKI resistance as a competitive decoy for miR‑149‑5p, thereby facilitating interleukin (IL)‑6 expression and inducing EMT‑like phenotypes. The knockdown or knockout of LINC00460 in gefitinib‑resistant non‑small cell lung cancer cells restored the response to EGFR‑TKI. In addition, as compared with patients with a low LINC00460 expression in tumors, those with a high LINC00460 expression had a significantly shorter progression‑free survival following gefitinib therapy, and a shorter overall survival. Therefore, LINC00460 may be a predictor of and potential therapeutic target for EGFR‑TKI resistance.