The relationship between miR-17-5p, miR-92a, and let-7b expression with non-small cell lung cancer targeted drug resistance.

PURPOSE To investigate the relationship between microRNA (miR)-17-5p, miR-92a, and let-7b expression and resistance to the non-small cell lung cancer (NSCLC) targeted drug Gefitinib. METHODS The human NSCLC cell line A549 and its drug resistant strain A549/GR (Gefitinib Resistant) was used in this study. The expression of miR-17-5p, miR-92a, and let-7b in different NSCLC cell lines was detected before and after transfection using real-time fluorescent PCR. Cell viability was detected using the CCK8 method. Cell cloning was performed to examine cell proliferation; cell apoptosis before and after transfection was evaluated using flow cytometry. RESULTS miR-17-5p and miR-92a expression in A549/ GR cells was 3.23 ± 0.92 and 9.29 ± 3.13 fold higher than in A549 cells respectively (p<0.05). In addition, let-7b expression in A549/GR cells was 29.37 ± 9.32% fold higher than in A549 cells (p<0.05). A549 cell sensitivity to Gefitinib was significantly decreased after transfection with the miR-17-5p mimic, miR-92a mimic, or the let-7b inhibitor (p<0.05), whereas the sensitivity of A549/GR cells to Gefitinib was significantly increased after transfection with miR-17-5p inhibitor, miR-92a inhibitor, or the let-7b mimic (p<0.05). A549 transfected with miR-17-5p mimic, miR- 92a mimic, and/or let-7b inhibitor formed more colonies than non-transfected controls (p<0.05); A549/GR transfected with miR-17-5p inhibitor, miR-92a inhibitor and let-7b mimic formed fewer colonies than the control group (p<0.05). The apoptosis rate of A549 cells transfected with miR-17-5p mimic, miR-92a mimic, or let-7b inhibitor was significantly lower than that of the control group (p<0.05); the apoptosis rate of A549/GR cells transfected with miR- 17-5p inhibitor, miR-92a inhibitor, or let-7b mimic was significantly higher than that of the control group (p<0.05). CONCLUSIONS Increased miR-17-5p and miR-92a expression and decreased let-7b expression can significantly induce proliferation and inhibit apoptosis of lung cancer cells, while reducing lung cancer cell sensitivity to Gefitinib.