MicroRNA (miR)‑27b has been reported to partici-pate in regulating the activity of non‑small cell lung carcinoma (NSCLC) cells. Additionally, when downregulated in NSCLC it promotes resistance to docetaxel; however, the underlying molecular mechanism remains largely unknown. Using reverse transcription‑quantitative polymerase chain reaction, the present study determined that the expression of miR‑27b was significantly reduced in NSCLC cells that were resistant to docetaxel. In addition, epidermal growth factor receptor (EGFR) was identified as a possible target of miR‑27b by searching the online miRNA database, TargetScan. A luciferase assay further validated EGFR as an effective target gene of miR‑27b. In addition, it was determined that in tumor tissue samples resistant to docetaxel miR‑27b was significantly downregulated, whilst EGFR was significantly upregulated. miR‑27b negatively regulated the expression of EGFR. This was evident as the transfection of miR‑27b mimics led to downregulation of the expression levels of EGFR, whilst miR‑27b inhibitors upregulated the expression levels of EGFR. Furthermore, it was demonstrated that the transfection of miR‑27b mimics significantly suppressed the apoptosis and promote the viability of A549 human lung carcinoma cells. In line with this, the introduction of miR‑27b inhibitors significantly induced apoptosis and inhibited the proliferation of A549 cells. These results indicate that miR‑27b may promote NSCLC cell viability and enhance resistance to docetaxel treatment through direct inhibition of EGFR expression. Additionally, miR‑27b may become a promising molecular target for improving the effectiveness of chemotherapy with docetaxel.