Abstract:Objective: To investigate the effect and mechanism of miR-217 on proliferation and apoptosis of non-small cell lung cancer cells. Methods: The expression levels of miR-217 and E2F3 mRNA in non-small cell lung cancer tissues and cells were detected by RT-qPCR.miR-NC, miR-217 mimic, miR-217 inhibitor, pc-NC, pc-E2F3 plasmids were transfected into non-small cell lung cancer SK-MES-1 or A549 cells, respectively or in combination, using Lipofectamine 2000. Cell proliferation was detected by clone formation experiments, apoptosis was detected by flow cytometry, targeting relationship was detected by dual luciferase report, and the relative expression level of E2F3 protein was detected by Western blot. Results: miR-217 was significantly down-regulated in non-small cell lung cancer tissues and cells (P<0.01). Compared with Control group, the number of cloned cells of SK-MES-1 or A549 cells in miR-217 mimic group significantly decreased, and the apoptosis rate increased significantly (P<0.01); the number of cloned cells of SK-MES-1 or A549 cells of non-small cell lung cancer in miR-217 inhibitor group significantly increased and the apoptosis rate decreased (P<0.01).miR-217 targeted down-regulation of E2F3. Co-transfection of pc-E2F3 reversed the effects of miR-217 on proliferation and apoptosis of non-small cell lung cancer SK-MES-1 or A549 cells. Conclusion: Overexpression of miR-217 inhibits the proliferation and induces apoptosis of non-small cell lung cancer SK-MES-1 or A549 cells by targeting E2F3.
