The Mechanism of Gas Anesthetics Affecting the Proliferation, Invasion and Metastasis of Osteosarcoma Cells and its Chemotherapy Sensitivity

Abstract

Zhang et al.: Gas Anesthetics Affecting the Osteosarcoma Cells and its Chemotherapy SensitivityTo explore the mechanism of gas anesthetics affecting osteosarcoma cell proliferation, invasion and metastasis of osteosarcoma cells and its chemotherapy sensitivity. We collected human osteosarcoma specimens from patients undergoing surgery. The expression of epithelial-to-mesenchymal transition process related proteins fibronectin, N-cadherin, E-cadherin and beta-catenin and the expression of apoptosis-related proteins B-cell lymphoma 2, caspase-9 and caspase-3 was analyzed by western blot. The cell proliferation of each group of cells was measured by cell counting kit-8. Transwell test were carried out to detect cell invasion and metastasis. The messenger RNA expression of phosphoinositide 3-kinase/protein kinase B pathway in cells was analyzed by quantitative reverse transcription polymerase chain reaction. The apoptosis was detected by Annexin V-FITC early apoptosis detection kit and cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide. Sevoflurane decreased the protein expression of N-cadherin and increased the protein expressions of E-cadherin and beta-catenin in a dosedependent manner (p<0.05). The low concentration group had decreased cell proliferation at 12 h, 24 h, 36 h and 72 h (p<0.05). The cell proliferation of the high concentration group decreased at 24 h, 36 h and 72 h (p<0.05). The sevoflurane reduced the number of cell invasion, cell metastasis and decreased the expression of B-cell lymphoma 2 protein in a dose-dependent manner (p<0.05). It increased the protein expressions of caspase-9 and caspase-3, reduced the messenger RNA expressions of phosphoinositide 3-kinase and protein kinase B and increased cell apoptosis and decreased cell viability in a dose-dependent manner (p<0.05). Gas anesthetic (sevoflurane) inhibited the proliferation, invasion and metastasis of osteosarcoma cells by inactivating the phosphoinositide 3-kinase/protein kinase B pathway and increased the chemotherapy sensitivity of osteosarcoma cells.