MECHANISM OF PROPOFOL IN INHIBITING EMT OF BREAST CANCER BY CONTROLLING MIR-21 EXPRESSION

Objective: To investigate the effect of propofol on MCR-7 cells of breast cancer and its possible regulatory mechanisms. Methods: The expression of miR-21 in breast cancer cells was examined by TCGA database analysis and real-time quantitative PCR. After overexpressed or knocked out miR-21 in breast cancer cells, the effect of miR-21 on the proliferation of breast cancer cells was measured by CCK-8 method. The effect of miR-21 on EMT expression in breast cancer cells was detected using Western blot and immunofluorescence staining, and the cell apoptosis was analyzed by flow cytometry. Results: It was confirmed that miR-21 was a downstream effector of propofol. Propofol inhibited the proliferation and migration of MCF-7 cells and significantly induced cell apoptosis. At the same time, propofol stimulated and inhibited miR-21 expression and EMT. When miR-21 was overexpressed, its effects on proliferation and apoptosis of MCF-7 cells as well as EMT were all attenuated. Furthermore, when propofol stimulated miR-21-depedent, the activation ofPI3K/AKT and Wnt3a/b-catenin pathways was reduced. Conclusion: Propofol inhibits MCF-7 cells proliferation and EMT by down-regulating the expression of miR-21. In addition, miR-21 can further regulate the PI3K/AKT and Wnt/b-catenin pathways.