Dexmetomidine promotes the activity of breast cancer cells through miR-199a/HIF-1α axis.

Abstract

BackgroundBreast cancer, as one of the most common malignant tumors in women, is still a great threat to women all over the world. Dexmetomidine (DMED) is a highly selective α2-adrenergic receptor agonist, which has attracted much attention in recent years. This study aimed to clarify the potential mechanism of DMED in regulating the activity of breast cancer cells.MethodsBreast cancer cell lines MCF-7 and MDA-MB-231 were treated with DMED. The levels of miR-199a and HIF-1α mRNA were detected using quantitative real-time polymerase chain reaction (QRT-PCR); the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and transwell assays were applied to monitor the activity of breast cancer cells; the apoptosis of breast cancer cells was detected using the caspase-3 activity assay and flow cytometry; binding of miR-199a and HIF-1α was assessed using double luciferase reporter gene assay, and western blot was employed to monitor the level of HIF-1α in cells.ResultsThe cytotoxicity and apoptosis of MCF-7 and MDA-MB-231 cells was inhibited by DMED. It also downregulated the expression of miR-199a in breast cancer cells and enhanced the downregulation of miR-199a to promote the activity of breast cancer cells and inhibit apoptosis. Also, miR-199a targeted HIF-1α. Further functional experiments confirmed that DMED promoted the progression of breast cancer through the miR-199a/HIF-1α axis.ConclusionsDMED promotes the activity of breast cancer cells through miR-199a/HIF-1αaxis. This can provide some reference for DMED in the clinical treatment of breast cancer.