BC enhanced resistance to EGFR‐tyrosine kinase inhibitors (EGFR‐TKIs) by activating the epithelial–mesenchymal transition. (A) (a) BC levels were determined by RT‐qPCR in A549 and 95D cells treated with EGF or VEGF. (b) BC levels were determined by RT‐qPCR in A549, 95C, 95D and PC9 cells treated with 2 μm/L gefitinib (24 h), vehicle or blank control. (c) BC expression was measured in PC9 cells treated with 2 μm/L erlotinib, afatinib or osimertinib. (B) BC expression was measured in gefitinib‐sensitive PC9 cells and gefitinib‐resistant PC9G cells from public microarray dataset GSE34228. IRS, gefitinib‐treatment. PC9GRM2, gefitinib‐resistance cell line. (C) (a and b) Viability of (a) BC‐overexpressing and (b) BC knockout PC9 cells was measured by the MTT assay after treatment with various concentrations of gefitinib (upper), afatinib (middle) or osimertinib (bottom) for 24 h. The IC50 of the EGFR‐TKIs was also measured. (D) The expression of cadherin, vimentin, Snai1, Slug, ZEB‐1 and AKT were determined by Western blot in 95C, 95D and A549 cells with BC overexpression. Data are represented as mean ± SEM of at least three independent experiments. *p < .05, **p < .01