Non-small cell lung cancer (NSCLC) poses a threat to human health and paclitaxel chemotherapy has been approved for the treatment of this type of cancer. However, resistance to treatment severely compromises the survival rate and prognosis of patients with NSCLC. The aim of the present study was to investigate the role of IL-1β in paclitaxel sensitivity of NSCLC cells and elucidate the underlying mechanism. The expression of IL-1β was found to be upregulated in NSCLC tissues and cells compared with healthy adjacent tissues and a normal epithelial cell line, respectively, as detected by reverse transcription-quantitative PCR and western blot analyses. Subsequently, Cell Counting Kit-8 assay and flow cytometry revealed that IL-1β weakened the sensitivity of A549 cells to paclitaxel. It was subsequently demonstrated that IL-1β induced A549 cell autophagy, while tunicamycin-induced autophagy increased the IL-1β expression level and weakened paclitaxel sensitivity. Thus, the results revealed that IL-1β reduced the sensitivity to paclitaxel in A549 cells by promoting autophagy and suggested that IL-1β may be of value for improving the therapeutic efficacy of paclitaxel chemotherapy in NSCLC.
Keywords: IL-1β; autophagy; drug sensitivity; non-small cell lung cancer; paclitaxel.
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