RESUMO
Objective: We aimed to explore the mechanism of microRNA-936 (miR-936) targeting G protein coupled receptor 78 (GPR78) regulating chemoresistance of non-small cell lung cancer (NSCLC) by activating the Galphaq Rho GTPase pathway. Methods: We added cisplatin to DMEM medium of HCC827/cisplatin cells and adjusted the final concentration to 1 µg/mL. Cells were divided into the control group and the miR-936 transfection group. Tissue samples were divided into the normal tissue group and the NSCLC tissue group. The mRNA expression of miR-936 in tissue samples was analyzed via reverse transcription polymerase chain reaction (RT-PCR). Cell migration and invasion were detected by wound healing assay. Cell counting kit 8 (CCK-8) was used to detect the cell viability 1, 2 and 3 days after cisplatin induction. The toxicity of cisplatin was analyzed by flow cytometry. The targeting relationship between miR-936 and GPR78 was detected by luciferase reporter gene assay. The regulation of miR-936 on GPR78/Rho GTPase was analyzed by Western blot. Results: The expression of miR-936 in NSCLC was lower than in normal tissues (P < .05). The number of cell migrations and invasions in the miR-936 transfection group was lower than in the control group (P < .05). The cell viability in the miR-936 transfection group was lower than in the control group on the 1st, 2nd and 3rd day (P < .05). With the increase in cisplatin concentration, the apoptosis rate of cells increased in a dependent manner (P < .05). Compared with GPR78 Mut, overexpression of miR-936 inhibited the luciferase activity of GPR78 WT 3'- UTR (P < .05). The expression of GPR78, RhoA, Rac1 and ABCB1 protein in the miR-936 transfection group was lower than in the control group (P < .05). The expression of GPR78 protein in the inhibitor+miR-936 transfection group was lower than in the inhibitor+control group (P < .05). Conclusion: miR-936 targets GPR78 and improves the sensitivity of NSCLC cells to cisplatin via the Galphaq Rho GTPase pathway.