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HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3

Glioblastoma (GBM) is the most prevalent and lethal type of primary malignant brain tumour. Recent studies suggest that the discovery of human cytomegalovirus (HCMV)-encoded microRNAs (miRNAs) might play a role in the pathogenesis of diseases, including GBM. In this study, we aimed to analyse the ex...

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Autores principales: Liang, Qing, Wang, Kejia, Wang, Bin, Cai, Qiliang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356197/
https://www.ncbi.nlm.nih.gov/pubmed/28303930
http://dx.doi.org/10.1038/srep44705
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author Liang, Qing
Wang, Kejia
Wang, Bin
Cai, Qiliang
author_facet Liang, Qing
Wang, Kejia
Wang, Bin
Cai, Qiliang
author_sort Liang, Qing
collection PubMed
description Glioblastoma (GBM) is the most prevalent and lethal type of primary malignant brain tumour. Recent studies suggest that the discovery of human cytomegalovirus (HCMV)-encoded microRNAs (miRNAs) might play a role in the pathogenesis of diseases, including GBM. In this study, we aimed to analyse the expression and function of HCMV-encoded miRNAs in GBM. We found that miR-UL112-3p expression was significantly elevated in GBM, and its expression levels were highly associated with glioma size, differentiation, WHO stage and the overall and disease-free survival of patients. The overexpression of miR-UL112-3p in the GBM cells promoted cell proliferation, clone formation, migration and invasion. In contrast, the down-regulation of miR-UL112-3p exerted an inverse effects. Tumour suppressor candidate 3 (TUSC3), a potential target gene of miR-UL112-3p, was inversely correlated with miR-UL112-3p expression in GBM tissues and cell lines. Furthermore, we demonstrated that TUSC3 was directly regulated by miR-UL112-3p, and the ectopic expression of TUSC3 reversed the effects of miR-UL112-3p on GBM progression via the AKT signalling pathway. Taken together, these findings collectively demonstrate that miR-UL112-3p exerts its oncogene function by directly targeting TUSC3 in GBM, indicating a potential novel therapeutic target for GBM.
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spelling pubmed-53561972017-03-22 HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3 Liang, Qing Wang, Kejia Wang, Bin Cai, Qiliang Sci Rep Article Glioblastoma (GBM) is the most prevalent and lethal type of primary malignant brain tumour. Recent studies suggest that the discovery of human cytomegalovirus (HCMV)-encoded microRNAs (miRNAs) might play a role in the pathogenesis of diseases, including GBM. In this study, we aimed to analyse the expression and function of HCMV-encoded miRNAs in GBM. We found that miR-UL112-3p expression was significantly elevated in GBM, and its expression levels were highly associated with glioma size, differentiation, WHO stage and the overall and disease-free survival of patients. The overexpression of miR-UL112-3p in the GBM cells promoted cell proliferation, clone formation, migration and invasion. In contrast, the down-regulation of miR-UL112-3p exerted an inverse effects. Tumour suppressor candidate 3 (TUSC3), a potential target gene of miR-UL112-3p, was inversely correlated with miR-UL112-3p expression in GBM tissues and cell lines. Furthermore, we demonstrated that TUSC3 was directly regulated by miR-UL112-3p, and the ectopic expression of TUSC3 reversed the effects of miR-UL112-3p on GBM progression via the AKT signalling pathway. Taken together, these findings collectively demonstrate that miR-UL112-3p exerts its oncogene function by directly targeting TUSC3 in GBM, indicating a potential novel therapeutic target for GBM. Nature Publishing Group 2017-03-17 /pmc/articles/PMC5356197/ /pubmed/28303930 http://dx.doi.org/10.1038/srep44705 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Liang, Qing
Wang, Kejia
Wang, Bin
Cai, Qiliang
HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3
title HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3
title_full HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3
title_fullStr HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3
title_full_unstemmed HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3
title_short HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3
title_sort hcmv-encoded mir-ul112-3p promotes glioblastoma progression via tumour suppressor candidate 3
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356197/
https://www.ncbi.nlm.nih.gov/pubmed/28303930
http://dx.doi.org/10.1038/srep44705
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