Abstract:
Objective: To explore the effect of miR-567 on the biological function and gefitinib resistance of nonsmall cell lung cancer (NSCLC).
Methods: Real-time fluorescence quantitative polymerase chain reaction (RTqPCR)was used to detect the expressions of miR-567 in human lung epithelial cell line BEAS-2B, non-small cell lung cancer cell line PC9, HCC827, A549, NCI-H1975, and gefitinib-resistant cell line PC9/GR.PC9 cells and PC9/GR cells were divided into negative control group, miR-567 mimic group, miR-567 inhibitor group and miR-567 mimic+CDK8 group, respectively.Cell proliferation ability was detected by CCK8 method, the migration and invasion ability of cells were detected by Transwell cell assay, the targeting relationship between miR-567 and CDK8 was detected by double luciferase reporter gene assay, and the expression of CDK8 in cells was detected by western blotting.
Results: The expression of miR-567 in PC9, HCC827, A549 and NCI-H1975 was significantly lower than that in BEAS-2B, and the expression of miR-567 in PC9/GR cells was significantly lower than that in PC9.Compared with negative control group, proliferation, migration and invasion ability of PC9 cells in miR-567 mimic group significantly decreased (
P<0.05) and those in miR-567 inhibitor group significantly increased (
P<0.05).The proliferation rate of PC9/GR cells in miR-567 mimic group was significantly lower than that in negative control group (
P<0.05), and the proliferation rate of PC9/GR cells in miR-567 inhibitor group was significantly higher than that in negative control group (
P<0.05).Double luciferase assay and western blotting analysis showed that CDK8 was the target gene of miR-567.Compared with miR-567 mimic group, proliferation, migration and invasion ability of PC9 cells in miR-567 mimic+CDK8 group significantly increased (
P<0.05), and the proliferation rate of PC9/GR cells significantly increased (
P<0.01).
Conclusion: miR-567 can inhibit proliferation, migration, invasion and gefitinib resistance of non-small cell lung cancer cells by targeting CDK8 regulation.