Propofol inhibits lung cancer cell viability and induces cell apoptosis by upregulating microRNA-486 expression

• Published in: Brazilian journal of medical and biological research Vol. 50; no. 1; p. e5794
• Main Authors: Yang, N, Liang, Y, Yang, P, Yang, T, Jiang, L
• Format: Journal Article
• Language: English; Portuguese
• Published: Brazil Associacao Brasileira de Divulgacao Cientifica (ABDC) 01.01.2017; Associação Brasileira de Divulgação Científica
• Subjects: Apoptosis; Apoptosis - drug effects; BIOLOGY; Biomedical Sciences; Cancer cells; Cell apoptosis; Cell Survival - drug effects; Cell viability; Dosage and administration; Drug therapy; Gene expression; Gene Expression Regulation, Neoplastic - drug effects; Genetic aspects; Humans; Lung cancer; Lung Neoplasms - metabolism; MEDICINE, RESEARCH & EXPERIMENTAL; microRNA-486; MicroRNAs - metabolism; Propofol; Propofol - pharmacology; Real-Time Polymerase Chain Reaction; Cell viability; microRNA-486; Propofol; Lung cancer; Cell apoptosis
• ISSN: 0100-879X; 1414-431X; 1414-431X
• DOI: 10.1590/1414-431x20165794

Propofol is a frequently used intravenous anesthetic agent. Recent studies show that propofol exerts a number of non-anesthetic effects. The present study aimed to investigate the effects of propofol on lung cancer cell lines H1299 and H1792 and functional role of microRNA (miR)-486 in these effects. H1299 and/or H1792 cells were treated with or without propofol and transfected or not with miR-486 inhibitor, and then cell viability and apoptosis were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry. The expression of miR-486 was determined by quantitative real-time polymerase chain reaction (qRT-PCR) with or without propofol treatment. Western blot was performed to analyze the protein expression of Forkhead box, class O (FOXO) 1 and 3, Bcl-2 interacting mediator of cell death (Bim), and pro- and activated caspases-3. Results showed that propofol significantly increased the miR-486 levels in both H1299 and H1792 cells compared to untreated cells in a dose-dependent manner (P<0.05 or P<0.01). Propofol statistically decreased cell viability but increased the percentages of apoptotic cells and protein expressions of FOXO1, FOXO3, Bim, and pro- and activated caspases-3; however, miR-486 inhibitor reversed the effects of propofol on cell viability, apoptosis, and protein expression (P<0.05 or P<0.01). In conclusion, propofol might be an ideal anesthetic for lung cancer surgery by effectively inhibiting lung cancer cell viability and inducing cell apoptosis. Modulation of miR-486 might contribute to the anti-tumor activity of propofol.