Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284 |
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Authors: | Wei-Zhen Liu Nian Liu |
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Institution: | Department of Anesthesia, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine,
Central South University, Changsha, P.R. China |
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Abstract: | Propofol has been widely used in lung cancer resections. Some studies have demonstrated that the effects
of propofol might be mediated by microRNAs (miRNAs). This study aimed to investigate the effects and
mechanisms of propofol on lung cancer cells by regulation of miR-1284. A549 cells were treated with different
concentrations of propofol, while transfected with miR-1284 inhibitor, si-FOXM1, and their negative controls.
Cell viability, migration, and invasion, and the expression of miR-1284, FOXM1, and epithelial–mesenchymal
transition (EMT) factors were detected by CCK-8, Transwell, qRT-PCR, and Western blot assays, respectively.
In addition, the regulatory and binding relationships among propofol, miR-1284, and FOXM1 were assessed,
respectively. Results showed that propofol suppressed A549 cell viability, migration, and invasion, upregulated
E-cadherin, and downregulated N-cadherin, vimentin, and Snail expressions. Moreover, propofol significantly
promoted the expression of miR-1284. miR-1284 suppression abolished propofol-induced decreases of cell
viability, migration, and invasion, and increased FOXM1 expression and the luciferase activity of FOXM1-wt.
Further, miR-1284 negatively regulated FOXM1 expression. FOXM1 knockdown reduced cell viability, migration, and invasion by propofol treatment plus miR-1284 suppression. In conclusion, our study indicated that
propofol could inhibit cell viability, migration, invasion, and the EMT process in lung cancer cells by regulation of miR-1284. |
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Keywords: | Propofol MicroRNA-1284 Cell viability Epithelial–mesenchymal transition (EMT) Migration Invasion |
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