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

• Published in: Brazilian journal of medical and biological research 2017-01, Vol.50 (1), p.e5794-e5794
• Main Authors: Yang, N, Liang, Y, Yang, P, Yang, T, Jiang, L
• Format: Article
• Language: English
• 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
• 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