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miR-543 functions as a tumor suppressor in glioma in vitro and in vivo

Gliomas are the most common primary central nervous system tumors and account for approximately 80% of malignant brain tumors. MicroRNAs (miRNAs) are a class of small non-coding, regulatory RNA molecules that mediate the expression levels of specific proteins. As a member of the miRNA family, miR-54...

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Autores principales: Xu, Liang, Yu, Ju, Wang, Zhongyong, Zhu, Qing, Wang, Wenjie, Lan, Qing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562083/
https://www.ncbi.nlm.nih.gov/pubmed/28627653
http://dx.doi.org/10.3892/or.2017.5712
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author Xu, Liang
Yu, Ju
Wang, Zhongyong
Zhu, Qing
Wang, Wenjie
Lan, Qing
author_facet Xu, Liang
Yu, Ju
Wang, Zhongyong
Zhu, Qing
Wang, Wenjie
Lan, Qing
author_sort Xu, Liang
collection PubMed
description Gliomas are the most common primary central nervous system tumors and account for approximately 80% of malignant brain tumors. MicroRNAs (miRNAs) are a class of small non-coding, regulatory RNA molecules that mediate the expression levels of specific proteins. As a member of the miRNA family, miR-543 plays a tumor suppressive or an oncogenic role in different types of tumors. However, the expression and role of miR-543 in glioma remain unknown. In the present study, the expression level of miR-543 in glioma cell lines and tissues was investigated. A series of in vitro and in vivo experiments was then performed to elucidate the function of miR-543 in glioma. Moreover, proteomic profiling was applied in this study to determine the landscape of differentially expressed proteins associated with miR-543-mediated carcinogenesis in glioma. We found that the expression level of miR-543 was greatly downregulated in glioma cell lines and tissues. Furthermore, the expression level of miR-543 was negatively associated with high-grade glioma. Functional studies demonstrated that miR-543 in glioma cells induced apoptosis and inhibited growth, the cell cycle, migration and invasion. In addition, the in vivo study showed that miR-543 suppressed tumorigenicity of glioma cells. In the present study, a label-free quantitative proteomic approach was performed and 339 proteins were identified as dysregulated after miR-543 was overexpressed. Among these dysregulated proteins, 165 were upregulated and 174 were downregulated. Moreover, multiple pathways were significantly enriched and were probably involved in miR-543-mediated tumorigenesis, including RNA degradation and the inositol phosphate metabolism pathway. In conclusion, miR-543 may function as a tumor suppressor in glioma and may serve as a future therapeutic target in therapy for patients with glioma.
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spelling pubmed-55620832017-11-02 miR-543 functions as a tumor suppressor in glioma in vitro and in vivo Xu, Liang Yu, Ju Wang, Zhongyong Zhu, Qing Wang, Wenjie Lan, Qing Oncol Rep Articles Gliomas are the most common primary central nervous system tumors and account for approximately 80% of malignant brain tumors. MicroRNAs (miRNAs) are a class of small non-coding, regulatory RNA molecules that mediate the expression levels of specific proteins. As a member of the miRNA family, miR-543 plays a tumor suppressive or an oncogenic role in different types of tumors. However, the expression and role of miR-543 in glioma remain unknown. In the present study, the expression level of miR-543 in glioma cell lines and tissues was investigated. A series of in vitro and in vivo experiments was then performed to elucidate the function of miR-543 in glioma. Moreover, proteomic profiling was applied in this study to determine the landscape of differentially expressed proteins associated with miR-543-mediated carcinogenesis in glioma. We found that the expression level of miR-543 was greatly downregulated in glioma cell lines and tissues. Furthermore, the expression level of miR-543 was negatively associated with high-grade glioma. Functional studies demonstrated that miR-543 in glioma cells induced apoptosis and inhibited growth, the cell cycle, migration and invasion. In addition, the in vivo study showed that miR-543 suppressed tumorigenicity of glioma cells. In the present study, a label-free quantitative proteomic approach was performed and 339 proteins were identified as dysregulated after miR-543 was overexpressed. Among these dysregulated proteins, 165 were upregulated and 174 were downregulated. Moreover, multiple pathways were significantly enriched and were probably involved in miR-543-mediated tumorigenesis, including RNA degradation and the inositol phosphate metabolism pathway. In conclusion, miR-543 may function as a tumor suppressor in glioma and may serve as a future therapeutic target in therapy for patients with glioma. D.A. Spandidos 2017-08 2017-06-12 /pmc/articles/PMC5562083/ /pubmed/28627653 http://dx.doi.org/10.3892/or.2017.5712 Text en Copyright: © Xu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Xu, Liang
Yu, Ju
Wang, Zhongyong
Zhu, Qing
Wang, Wenjie
Lan, Qing
miR-543 functions as a tumor suppressor in glioma in vitro and in vivo
title miR-543 functions as a tumor suppressor in glioma in vitro and in vivo
title_full miR-543 functions as a tumor suppressor in glioma in vitro and in vivo
title_fullStr miR-543 functions as a tumor suppressor in glioma in vitro and in vivo
title_full_unstemmed miR-543 functions as a tumor suppressor in glioma in vitro and in vivo
title_short miR-543 functions as a tumor suppressor in glioma in vitro and in vivo
title_sort mir-543 functions as a tumor suppressor in glioma in vitro and in vivo
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562083/
https://www.ncbi.nlm.nih.gov/pubmed/28627653
http://dx.doi.org/10.3892/or.2017.5712
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