Breast cancer is a common malignant tumor with a high incidence of recurrence and metastasis. It has been reported that propofol has certain anti-breast cancer effects, but the intrinsic molecular mechanism remains unclear. This study investigated the effect of propofol on breast cancer MCF-7 cells and its possible regulatory mechanisms. MCF-7 cells were treated by propofol, and then the effects of propofol on cell growth and epithelial-mesenchymal transition (EMT) were studied. We subsequently testified whether miR-21 was a downstream effector of propofol. As a result, propofol repressed the proliferation and migration of MCF-7 cells, but significantly induced apoptosis. Meanwhile, miR-21 expression and EMT were inhibited by propofol stimulation. The effects of propofol on MCF-7 cells proliferation, apoptosis and EMT were all attenuated when miR-21 was overexpressed. Besides this, the activation of PI3K/AKT and Wnt3a/β-catenin pathways was reduced by propofol stimulation in a miR-21-depedent manner. In conclusion, propofol can inhibit the proliferation and EMT of MCF-7 cells by down-regulating miR-21 expression. Moreover, miR-21 can further regulate PI3K/AKT and Wnt/β-catenin pathways.
Keywords: MCF-7; Propofol; epithelial-mesenchymal transition (EMT); miR-21.