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MiR-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5
Glioblastoma is one of the most common malignant primary tumors and develops in brain. The molecular mechanism that regulates glioblastoma occurrence still remains unknown. MicroRNA (miR)-500a-5p has been reported to be involved in hepatocellular carcinoma and breast cancer. Whether miR-500a-5p regu...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6102694/ https://www.ncbi.nlm.nih.gov/pubmed/30015879 http://dx.doi.org/10.3892/mmr.2018.9259 |
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author | Liu, Zhiyong Su, Danying Qi, Xiuying Ma, Jing |
author_facet | Liu, Zhiyong Su, Danying Qi, Xiuying Ma, Jing |
author_sort | Liu, Zhiyong |
collection | PubMed |
description | Glioblastoma is one of the most common malignant primary tumors and develops in brain. The molecular mechanism that regulates glioblastoma occurrence still remains unknown. MicroRNA (miR)-500a-5p has been reported to be involved in hepatocellular carcinoma and breast cancer. Whether miR-500a-5p regulates glioblastoma progression requires further investigation. In the present study, miR-500a-5p was highly expressed in malignant glioblastoma tissues and cell lines. Overexpression of miR-500a-5p promoted glioblastoma cell proliferation, migration and invasion in vitro. In addition, knockdown of miR-500a-5p accelerated cell apoptosis. Furthermore, miR-500a-5p inhibition significantly impaired tumor growth in vivo. The present study further explored the downstream mechanism. The luciferase reporter assay revealed that miR-500a-5p directly binds the 3′-untranslated region of chromodomain helicase DNA binding protein 5 (CHD5) mRNA. MiR-500a-5p markedly inhibited CHD5 expression in glioblastoma cells. Furthermore, CHD5 was downregulated in glioblastoma tissues, and the expression levels of miR-500a-5p and CHD5 were inversely correlated. In addition, knockdown of CHD5 restored the inhibition of cell proliferation and migration triggered by miR-500a-5p silence. Finally, it was demonstrated that miR-500a-5p can serve as a novel biomarker for the diagnosis and prognosis of glioblastoma patients. Taken together, the results of the present study indicated that miR-500a-5p may have promoted glioblastoma development and progression by targeting CHD5. |
format | Online Article Text |
id | pubmed-6102694 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-61026942018-08-23 MiR-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5 Liu, Zhiyong Su, Danying Qi, Xiuying Ma, Jing Mol Med Rep Articles Glioblastoma is one of the most common malignant primary tumors and develops in brain. The molecular mechanism that regulates glioblastoma occurrence still remains unknown. MicroRNA (miR)-500a-5p has been reported to be involved in hepatocellular carcinoma and breast cancer. Whether miR-500a-5p regulates glioblastoma progression requires further investigation. In the present study, miR-500a-5p was highly expressed in malignant glioblastoma tissues and cell lines. Overexpression of miR-500a-5p promoted glioblastoma cell proliferation, migration and invasion in vitro. In addition, knockdown of miR-500a-5p accelerated cell apoptosis. Furthermore, miR-500a-5p inhibition significantly impaired tumor growth in vivo. The present study further explored the downstream mechanism. The luciferase reporter assay revealed that miR-500a-5p directly binds the 3′-untranslated region of chromodomain helicase DNA binding protein 5 (CHD5) mRNA. MiR-500a-5p markedly inhibited CHD5 expression in glioblastoma cells. Furthermore, CHD5 was downregulated in glioblastoma tissues, and the expression levels of miR-500a-5p and CHD5 were inversely correlated. In addition, knockdown of CHD5 restored the inhibition of cell proliferation and migration triggered by miR-500a-5p silence. Finally, it was demonstrated that miR-500a-5p can serve as a novel biomarker for the diagnosis and prognosis of glioblastoma patients. Taken together, the results of the present study indicated that miR-500a-5p may have promoted glioblastoma development and progression by targeting CHD5. D.A. Spandidos 2018-09 2018-07-09 /pmc/articles/PMC6102694/ /pubmed/30015879 http://dx.doi.org/10.3892/mmr.2018.9259 Text en Copyright: © Liu 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 Liu, Zhiyong Su, Danying Qi, Xiuying Ma, Jing MiR-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5 |
title | MiR-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5 |
title_full | MiR-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5 |
title_fullStr | MiR-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5 |
title_full_unstemmed | MiR-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5 |
title_short | MiR-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase DNA binding protein 5 |
title_sort | mir-500a-5p promotes glioblastoma cell proliferation, migration and invasion by targeting chromodomain helicase dna binding protein 5 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6102694/ https://www.ncbi.nlm.nih.gov/pubmed/30015879 http://dx.doi.org/10.3892/mmr.2018.9259 |
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