Abstract
BACKGROUND: Breast 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. METHODS: Breast 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. RESULTS: The 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. CONCLUSIONS: DMED 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.