The Effect of Sevoflurane on the Proliferation, Epithelial-Mesenchymal Transition (EMT) and Apoptosis in Human Breast Cancer Cells

Abstract

Background: The common inhalational anaesthetuc sevoflurane has been implicated in tumorigenesis. This study explored its effect on proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) in MCF-7 human breast cancer cells. Methods: MCF-7 cell lines were treated with different gradient concentrations of sevoflurane for 6 h. EdU-based proliferation assay and detection by immunoblotting of several proliferation-associated proteins including p21, proliferating cell nuclear antigen (PCNA), and cyclinD1, were employed to determine the influence of sevoflurane on proliferation. Flow cytometry assay and immunoblotting assay were used to analyze cellular apoptosis and apoptosis-relevant proteins;containing Bcl-2, Bax, cleaved-caspase-3, cleaved-caspase-9, as well as cleaved-PARP1, EMT-associated markers contain N-cadherin, E-cadherin, β-catenin, vimentin and discoidin domain receptor 2 (DDR2) as well as janus kinase 2 (JAK2), p-JAK2, signal transducer and activator of transcription-3 (STAT3) and p-STAT3. Transwell assay was conducted to evaluate the cells invasion. Results: The results suggested that sevoflurane restrained the proliferation and EMT, but promoted the apoptosis of MCF-7 cells. Besides, sevoflurane treatment contributes to the downregulation of the JAK2/STAT3 pathway. RO8191 (a JAK2 activator) weakened the effects of sevoflurane on proliferation, apoptosis, and EMT in MCF-7 cells. Conclusions: To sum up, sevoflurane suppresses proliferation and EMT and promotes apoptosis by repressing the JAK2/STAT3 pathway in MCF-7 cells.