Aurora A is a member of the mitotic serine/threonine kinase family. It is involved in key processes during mitosis and meiosis, and Aurora A upregulation is implicated in malignant transformation. In the present study, we revealed that Aurora A expression was significantly higher in docetaxel‑resistant lung adenocarcinoma (LAD) cells than in parental cells. Higher levels of Aurora A expression were significantly correlated with higher chemoresistance and proliferation in LAD cells, while silencing Aurora A promoted caspase‑3‑dependent cell apoptosis by downregulating NF‑κB and Bcl‑2 and upregulating Bax expression. In addition, an increased proportion of cells in the G2/M phase and a decreased proportion of cells in the S phase were observed due to the suppression of Aurora A. Furthermore, we identified that microRNA‑885‑3p (miR‑885‑3p) could target Aurora A directly. There was significantly lower miR‑885‑3p expression in docetaxel‑resistant LAD cells than in parental LAD cells. miR‑885‑3p could modulate the docetaxel response, cell proliferation and apoptosis in LAD cells in vitro. Moreover, we found that Aurora A overexpression or miR‑885‑3p inhibition was associated with more aggressive behaviour in LAD cells. Thus, miR‑885‑3p/Aurora A may be involved in the chemoresistance of LAD cells, and assessing miR‑885‑3p/Aurora A expression may be a potential method for indicating chemosensitivity to docetaxel‑based chemotherapy.