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miR-525-5p Modulates Proliferation and Epithelial–Mesenchymal Transition of Glioma by Targeting Stat-1
BACKGROUND: Glioma is the most aggressive human brain tumor. Recent studies revealed that microRNAs play vital roles in glioma. However, the function of microRNA-525-5p (miR-525-5p) in glioma remains unclear. METHODS: qRT-PCR and Western blotting were used to evaluate mRNA and protein levels in glio...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7548333/ https://www.ncbi.nlm.nih.gov/pubmed/33116581 http://dx.doi.org/10.2147/OTT.S257951 |
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author | Xie, Peng Han, Qiu Liu, Dachao Yao, Dan Lu, Xiaoqing Wang, Ziyu Zuo, Xiaohua |
author_facet | Xie, Peng Han, Qiu Liu, Dachao Yao, Dan Lu, Xiaoqing Wang, Ziyu Zuo, Xiaohua |
author_sort | Xie, Peng |
collection | PubMed |
description | BACKGROUND: Glioma is the most aggressive human brain tumor. Recent studies revealed that microRNAs play vital roles in glioma. However, the function of microRNA-525-5p (miR-525-5p) in glioma remains unclear. METHODS: qRT-PCR and Western blotting were used to evaluate mRNA and protein levels in glioma tissues and cells. Colony formation, CCK-8, and Edu assays evaluated the growth of glioma cells. Wound-healing, transwell, and 3D invasion assays examined the migration and invasion activities of glioma cells. Luciferase reporter assays assessed the regulatory relationship interaction between miR-525-5p and Stat-1. A mouse xenograft model was used to examine the effect of miR-525-5p on glioma in vivo. RESULTS: miR-525-5p expression was downregulated in glioma tissues and cells. Overexpressing miR-525-5p decreased the growth of glioma cells and reduced the migration, invasion, and epithelial–mesenchymal transition of glioma cells. Bioinformatics analysis identified Stat-1 as a potential target of miR-525-5p, and dual luciferase reporter assays revealed that miR-525-5p negatively regulates Stat-1. Decreased Stat-1 led to the inhibition of FOXM1, affecting NF-κB signaling activity. Overexpressing miR-525-5p reduced tumor development in vivo. CONCLUSION: miR-525-5p negatively regulates cell proliferation, migration, invasion, and epithelial–mesenchymal transition in glioma, and Stat 1 is a target of miR-525-5p. miR-525-5p may be a potential target for glioma treatment. |
format | Online Article Text |
id | pubmed-7548333 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-75483332020-10-27 miR-525-5p Modulates Proliferation and Epithelial–Mesenchymal Transition of Glioma by Targeting Stat-1 Xie, Peng Han, Qiu Liu, Dachao Yao, Dan Lu, Xiaoqing Wang, Ziyu Zuo, Xiaohua Onco Targets Ther Original Research BACKGROUND: Glioma is the most aggressive human brain tumor. Recent studies revealed that microRNAs play vital roles in glioma. However, the function of microRNA-525-5p (miR-525-5p) in glioma remains unclear. METHODS: qRT-PCR and Western blotting were used to evaluate mRNA and protein levels in glioma tissues and cells. Colony formation, CCK-8, and Edu assays evaluated the growth of glioma cells. Wound-healing, transwell, and 3D invasion assays examined the migration and invasion activities of glioma cells. Luciferase reporter assays assessed the regulatory relationship interaction between miR-525-5p and Stat-1. A mouse xenograft model was used to examine the effect of miR-525-5p on glioma in vivo. RESULTS: miR-525-5p expression was downregulated in glioma tissues and cells. Overexpressing miR-525-5p decreased the growth of glioma cells and reduced the migration, invasion, and epithelial–mesenchymal transition of glioma cells. Bioinformatics analysis identified Stat-1 as a potential target of miR-525-5p, and dual luciferase reporter assays revealed that miR-525-5p negatively regulates Stat-1. Decreased Stat-1 led to the inhibition of FOXM1, affecting NF-κB signaling activity. Overexpressing miR-525-5p reduced tumor development in vivo. CONCLUSION: miR-525-5p negatively regulates cell proliferation, migration, invasion, and epithelial–mesenchymal transition in glioma, and Stat 1 is a target of miR-525-5p. miR-525-5p may be a potential target for glioma treatment. Dove 2020-10-07 /pmc/articles/PMC7548333/ /pubmed/33116581 http://dx.doi.org/10.2147/OTT.S257951 Text en © 2020 Xie et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Xie, Peng Han, Qiu Liu, Dachao Yao, Dan Lu, Xiaoqing Wang, Ziyu Zuo, Xiaohua miR-525-5p Modulates Proliferation and Epithelial–Mesenchymal Transition of Glioma by Targeting Stat-1 |
title | miR-525-5p Modulates Proliferation and Epithelial–Mesenchymal Transition of Glioma by Targeting Stat-1 |
title_full | miR-525-5p Modulates Proliferation and Epithelial–Mesenchymal Transition of Glioma by Targeting Stat-1 |
title_fullStr | miR-525-5p Modulates Proliferation and Epithelial–Mesenchymal Transition of Glioma by Targeting Stat-1 |
title_full_unstemmed | miR-525-5p Modulates Proliferation and Epithelial–Mesenchymal Transition of Glioma by Targeting Stat-1 |
title_short | miR-525-5p Modulates Proliferation and Epithelial–Mesenchymal Transition of Glioma by Targeting Stat-1 |
title_sort | mir-525-5p modulates proliferation and epithelial–mesenchymal transition of glioma by targeting stat-1 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7548333/ https://www.ncbi.nlm.nih.gov/pubmed/33116581 http://dx.doi.org/10.2147/OTT.S257951 |
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