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Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284

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...

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Autores principales: Liu, Wei-Zhen, Liu, Nian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cognizant Communication Corporation 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848461/
https://www.ncbi.nlm.nih.gov/pubmed/29402342
http://dx.doi.org/10.3727/096504018X15172738893959
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author Liu, Wei-Zhen
Liu, Nian
author_facet Liu, Wei-Zhen
Liu, Nian
author_sort Liu, Wei-Zhen
collection PubMed
description 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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spelling pubmed-78484612021-02-16 Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284 Liu, Wei-Zhen Liu, Nian Oncol Res Article 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. Cognizant Communication Corporation 2018-12-27 /pmc/articles/PMC7848461/ /pubmed/29402342 http://dx.doi.org/10.3727/096504018X15172738893959 Text en Copyright © 2019 Cognizant, LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This article is licensed under a Creative Commons Attribution-NonCommercial NoDerivatives 4.0 International License.
spellingShingle Article
Liu, Wei-Zhen
Liu, Nian
Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284
title Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284
title_full Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284
title_fullStr Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284
title_full_unstemmed Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284
title_short Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284
title_sort propofol inhibits lung cancer a549 cell growth and epithelial–mesenchymal transition process by upregulation of microrna-1284
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848461/
https://www.ncbi.nlm.nih.gov/pubmed/29402342
http://dx.doi.org/10.3727/096504018X15172738893959
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