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Targeting microRNA-23a to inhibit glioma cell invasion via HOXD10

Glioma is the most frequent primary brain tumor. Recently, the upregulation of microRNA (miR)-23a was found to be associated with glioma, but the molecular mechanism by which miR-23a promotes glioma growth remains to be unveiled. In the present study, we found that miR-23a was significantly upregula...

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Detalles Bibliográficos
Autores principales: Hu, Xing, Chen, Dan, Cui, Yanhui, Li, Zhiyuan, Huang, Jufang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3851882/
https://www.ncbi.nlm.nih.gov/pubmed/24305689
http://dx.doi.org/10.1038/srep03423
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author Hu, Xing
Chen, Dan
Cui, Yanhui
Li, Zhiyuan
Huang, Jufang
author_facet Hu, Xing
Chen, Dan
Cui, Yanhui
Li, Zhiyuan
Huang, Jufang
author_sort Hu, Xing
collection PubMed
description Glioma is the most frequent primary brain tumor. Recently, the upregulation of microRNA (miR)-23a was found to be associated with glioma, but the molecular mechanism by which miR-23a promotes glioma growth remains to be unveiled. In the present study, we found that miR-23a was significantly upregulated in glioma tissues compared to their matched adjacent tissues. miR-23a was also highly expressed in glioma cell lines SHG44, U251, and U87 cells. Moreover, we identified homeobox D10 (HOXD10) as a novel target for miR-23a. The expression of HOXD10 was significantly reduced in glioma tissues and cell lines, and miR-23a negatively regulates the protein expression of HOXD10 in U251 and U87 cells. We further showed that miRNA-23a promoted U251 and U87 cell invasion, at least partially, by directly targeting HOXD10 and further modulating MMP-14. These findings suggest that miR-23a may serve as a promising therapeutic target for glioma.
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spelling pubmed-38518822013-12-05 Targeting microRNA-23a to inhibit glioma cell invasion via HOXD10 Hu, Xing Chen, Dan Cui, Yanhui Li, Zhiyuan Huang, Jufang Sci Rep Article Glioma is the most frequent primary brain tumor. Recently, the upregulation of microRNA (miR)-23a was found to be associated with glioma, but the molecular mechanism by which miR-23a promotes glioma growth remains to be unveiled. In the present study, we found that miR-23a was significantly upregulated in glioma tissues compared to their matched adjacent tissues. miR-23a was also highly expressed in glioma cell lines SHG44, U251, and U87 cells. Moreover, we identified homeobox D10 (HOXD10) as a novel target for miR-23a. The expression of HOXD10 was significantly reduced in glioma tissues and cell lines, and miR-23a negatively regulates the protein expression of HOXD10 in U251 and U87 cells. We further showed that miRNA-23a promoted U251 and U87 cell invasion, at least partially, by directly targeting HOXD10 and further modulating MMP-14. These findings suggest that miR-23a may serve as a promising therapeutic target for glioma. Nature Publishing Group 2013-12-05 /pmc/articles/PMC3851882/ /pubmed/24305689 http://dx.doi.org/10.1038/srep03423 Text en Copyright © 2013, Macmillan Publishers Limited. All rights reserved http://creativecommons.org/licenses/by/3.0/ This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/
spellingShingle Article
Hu, Xing
Chen, Dan
Cui, Yanhui
Li, Zhiyuan
Huang, Jufang
Targeting microRNA-23a to inhibit glioma cell invasion via HOXD10
title Targeting microRNA-23a to inhibit glioma cell invasion via HOXD10
title_full Targeting microRNA-23a to inhibit glioma cell invasion via HOXD10
title_fullStr Targeting microRNA-23a to inhibit glioma cell invasion via HOXD10
title_full_unstemmed Targeting microRNA-23a to inhibit glioma cell invasion via HOXD10
title_short Targeting microRNA-23a to inhibit glioma cell invasion via HOXD10
title_sort targeting microrna-23a to inhibit glioma cell invasion via hoxd10
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3851882/
https://www.ncbi.nlm.nih.gov/pubmed/24305689
http://dx.doi.org/10.1038/srep03423
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