Upregulation of miR-202-3p reverses Icotinib resistance in lung carcinoma A549/Ico cells

Objective(s): Icotinib exerts a good anti-tumor efficacy on non-small cell lung cancer (NSCLC), while Icotinib resistance has become an important limiting factor in the clinical application. Studies have certified that a great quantity of microRNAs are involved in the development of cancer. The aim of present study is to investigate whether miR-202-3p reduces Icotinib resistance in lung carcinoma A549/Ico cells. Materials and Methods: Icotinib-resistant A549/Ico cells was established in the previous stage. The levels of miR-202-3p in A549 and A549/Ico cells were detected by qRT-PCR. The IC50 of A549 and A549/Ico cells were detected by MTT assay. The mRNA and protein levels of ADP-Ribosylation Factor-like 5A (ARL5A), the functional target of miR-202-3p, as well as the multi-drug resistant (MDR) related genes glutathione s transferase pi (GST-pi), Multi Drug Resistance 1 (MDR1), multidrug resistance-associated protein 1 (MRP1) and breast cancer resistance protein (BCRP) were measured by qRT-PCR and western blot. Results: miR-202-3p was observably down-regulated in A549/Ico cells. Transfection of A549/Ico cells with miR-202-3p reversed the Icotinib resistance and increased cell apoptosis. The levels of ARL5A, GST-p, MDR1, MRP1 and BCRP were significantly down-regulated following the upregulation of miR-202-3p in A549/Ico cells. Conclusion: Our study demonstrated that miR-202-3p transfection reduced Icotinib resistance in A549/Ico cells, which could be by its downstream target ARL5A and MDR-related genes. These findings suggest that miR-202-3p may function as a novel therapeutic candidate in patients with MDR lung cancer.