Fig. 3

miR-762 upregulation desensitizes NSCLC cells to gefitinib treatment. a 48 h after transfection with miR-762 inhibitors or negative controls (NC), PC-9/GR and A549/GR cells were subjected to RT-qPCR analysis of miR-762 expression. b PC-9/GR and A549/GR cells were treated with different doses of gefitinib (8 μM for PC-9/GR, 60 μM for A549/GR) for 24 or 48 h. Cell viability was assayed using a MTT Assay Kit at 590 nm (*P < 0.05 and **P < 0.01). c Cells were treated with different doses of gefitinib (8 μM for PC-9/GR, 60 μM for A549/GR) for 24 or 48 h. Cell apoptosis was assayed using an ApoStrand™ ELISA Apoptosis Detection Kit at 405 nm (*P < 0.05 and **P < 0.01). d In vivo gefitinib sensitivity was evaluated using a xenograft model, as described in Materials and methods. Tumor volume was measured and recorded once a week (*P < 0.05 and ** P < 0.01 when comparing Inhibitors + vehicle to Inhibitors + gefitinib). e 48 h after transfection with miR-762 mimics or Mimics-NC, PC-9 and A549 cells were subjected to RT-qPCR analysis of miR-762 expression. f PC-9 and A549 cells were treated with different doses of gefitinib (0.2 μM for PC-9 and 12.5 μM for A549 cells) for 24 or 48 h. Cell viability was assayed using a MTT Assay Kit at 590 nm (*P < 0.05 and **P < 0.01). g PC-9 and A549 cells were treated with different doses of gefitinib (0.2 μM for PC-9 and 12.5 μM for A549 cells) for 24 or 48 h. Cell apoptosis was assayed using an ApoStrand™ ELISA Apoptosis Detection Kit at 405 nm (*P < 0.05 and **P < 0.01). h In vivo gefitinib sensitivity was evaluated using a xenograft model, as described in Materials and methods. Tumor volume was measured and recorded once a week (*P < 0.05 and **P < 0.01 when comparing Mimics + vehicle to Mimics + gefitinib)