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MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9
Glioblastoma multiforme (GBM) is the most common primary malignant tumors originating in the brain parenchyma. At present, GBM patients have a poor prognosis despite the continuous progress in therapeutic technologies including surgery, radiotherapy, photodynamic therapy, and chemotherapy. Recent st...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386681/ https://www.ncbi.nlm.nih.gov/pubmed/27911279 http://dx.doi.org/10.18632/oncotarget.13706 |
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author | Liu, Nan Zhang, Lei Wang, Zhen Cheng, Yingduan Zhang, Pengxing Wang, Xin Wen, Weihong Yang, Hongwei Liu, Hui Jin, Weilin Zhang, Yongsheng Tu, Yanyang |
author_facet | Liu, Nan Zhang, Lei Wang, Zhen Cheng, Yingduan Zhang, Pengxing Wang, Xin Wen, Weihong Yang, Hongwei Liu, Hui Jin, Weilin Zhang, Yongsheng Tu, Yanyang |
author_sort | Liu, Nan |
collection | PubMed |
description | Glioblastoma multiforme (GBM) is the most common primary malignant tumors originating in the brain parenchyma. At present, GBM patients have a poor prognosis despite the continuous progress in therapeutic technologies including surgery, radiotherapy, photodynamic therapy, and chemotherapy. Recent studies revealed that miR-101 was remarkably down-regulated in kinds of human cancers and was associated with aggressive tumor cell proliferation and stem cell self-renewal. Data also showed that miR-101 was down-regulated in primary glioma samples and cell lines, but the underlying molecular mechanism of the deregulation of miR-101 in glioma remained largely unknown. In this study, we found that miR-101 could inhibit the proliferation and invasion of glioma cells both in vitro and in vivo by directly targeting SOX9 [sex-determining region Y (SRY)-box9 protein]. Silencing of SOX9 exerted similar effects with miR-101 overexpression on glioma cells proliferation and invasion. Quantitative reverse transcription PCR and Western blotting analysis revealed a negative relationship between miR-101 and SOX9 in human glioma U251MG and U87MG cells, and the luciferase assay indicated that miR-101 altered SOX9 expression by directly targeting on 3′UTR. Taken together, our findings suggest that miR-101 regulates glioma proliferation, migration and invasion via directly down-regulating SOX9 both in vitro and in vivo, and miR-101 may be a potential therapeutic target for future glioma treatment. |
format | Online Article Text |
id | pubmed-5386681 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-53866812017-04-26 MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9 Liu, Nan Zhang, Lei Wang, Zhen Cheng, Yingduan Zhang, Pengxing Wang, Xin Wen, Weihong Yang, Hongwei Liu, Hui Jin, Weilin Zhang, Yongsheng Tu, Yanyang Oncotarget Research Paper Glioblastoma multiforme (GBM) is the most common primary malignant tumors originating in the brain parenchyma. At present, GBM patients have a poor prognosis despite the continuous progress in therapeutic technologies including surgery, radiotherapy, photodynamic therapy, and chemotherapy. Recent studies revealed that miR-101 was remarkably down-regulated in kinds of human cancers and was associated with aggressive tumor cell proliferation and stem cell self-renewal. Data also showed that miR-101 was down-regulated in primary glioma samples and cell lines, but the underlying molecular mechanism of the deregulation of miR-101 in glioma remained largely unknown. In this study, we found that miR-101 could inhibit the proliferation and invasion of glioma cells both in vitro and in vivo by directly targeting SOX9 [sex-determining region Y (SRY)-box9 protein]. Silencing of SOX9 exerted similar effects with miR-101 overexpression on glioma cells proliferation and invasion. Quantitative reverse transcription PCR and Western blotting analysis revealed a negative relationship between miR-101 and SOX9 in human glioma U251MG and U87MG cells, and the luciferase assay indicated that miR-101 altered SOX9 expression by directly targeting on 3′UTR. Taken together, our findings suggest that miR-101 regulates glioma proliferation, migration and invasion via directly down-regulating SOX9 both in vitro and in vivo, and miR-101 may be a potential therapeutic target for future glioma treatment. Impact Journals LLC 2016-11-30 /pmc/articles/PMC5386681/ /pubmed/27911279 http://dx.doi.org/10.18632/oncotarget.13706 Text en Copyright: © 2017 Liu et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Liu, Nan Zhang, Lei Wang, Zhen Cheng, Yingduan Zhang, Pengxing Wang, Xin Wen, Weihong Yang, Hongwei Liu, Hui Jin, Weilin Zhang, Yongsheng Tu, Yanyang MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9 |
title | MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9 |
title_full | MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9 |
title_fullStr | MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9 |
title_full_unstemmed | MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9 |
title_short | MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9 |
title_sort | microrna-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting sox9 |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386681/ https://www.ncbi.nlm.nih.gov/pubmed/27911279 http://dx.doi.org/10.18632/oncotarget.13706 |
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