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Roles of microRNA-99 family in human glioma
OBJECTIVE: Deregulation of microRNA (miR)-99 family members (miR-99a, miR-99b, and miR-100) has been reported to play a crucial role in many cancer types. However, their roles in human gliomas have not been fully elucidated. This study aimed to investigate the expression patterns of miR-99a, miR-99b...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4920231/ https://www.ncbi.nlm.nih.gov/pubmed/27382299 http://dx.doi.org/10.2147/OTT.S99363 |
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author | Zhang, Mingyu Guo, Yong Wu, Jun Chen, Fenghua Dai, Zhijie Fan, Shuangshi Li, Pengcheng Song, Tao |
author_facet | Zhang, Mingyu Guo, Yong Wu, Jun Chen, Fenghua Dai, Zhijie Fan, Shuangshi Li, Pengcheng Song, Tao |
author_sort | Zhang, Mingyu |
collection | PubMed |
description | OBJECTIVE: Deregulation of microRNA (miR)-99 family members (miR-99a, miR-99b, and miR-100) has been reported to play a crucial role in many cancer types. However, their roles in human gliomas have not been fully elucidated. This study aimed to investigate the expression patterns of miR-99a, miR-99b, and miR-100 in glioma tissues and to evaluate their expression profiles with respect to tumor progression. METHODS: Quantitative real-time polymerase chain reaction was performed to detect the expression levels of miR-99a, miR-99b, and miR-100 in glioma and matched non-neoplastic brain tissues. Then, the associations of their expression with various clinicopathological features of glioma patients were statistically analyzed. Moreover, the roles of miR-99a, miR-99b, and miR-100 in regulating glioma cell migration and invasion were determined via transwell assay in vitro. RESULTS: Compared with non-neoplastic brain tissues, miR-99a, miR-99b, and miR-100 expression levels were all significantly decreased in glioma tissues (all P<0.001). miR-99a-low, miR-99b-low, and miR-100-low expression more frequently occurred in glioma patients with low Karnofsky performance score (<90) and high World Health Organization grade (III–IV). Further functional experiments revealed that the enforced expression of miR-99a, miR-99b, and miR-100 resulted in the inhibition of cellular migration and invasion in glioma cells. CONCLUSION: Our results strongly suggest that the aberrant expression of miR-99a, miR-99b, and miR-100 may be a common feature in human gliomas with aggressive clinicopathological features and may participate in malignant phenotypes of the tumors. These findings highlight the potential of the three miR-99 family members as novel therapeutic targets for human gliomas. |
format | Online Article Text |
id | pubmed-4920231 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-49202312016-07-05 Roles of microRNA-99 family in human glioma Zhang, Mingyu Guo, Yong Wu, Jun Chen, Fenghua Dai, Zhijie Fan, Shuangshi Li, Pengcheng Song, Tao Onco Targets Ther Original Research OBJECTIVE: Deregulation of microRNA (miR)-99 family members (miR-99a, miR-99b, and miR-100) has been reported to play a crucial role in many cancer types. However, their roles in human gliomas have not been fully elucidated. This study aimed to investigate the expression patterns of miR-99a, miR-99b, and miR-100 in glioma tissues and to evaluate their expression profiles with respect to tumor progression. METHODS: Quantitative real-time polymerase chain reaction was performed to detect the expression levels of miR-99a, miR-99b, and miR-100 in glioma and matched non-neoplastic brain tissues. Then, the associations of their expression with various clinicopathological features of glioma patients were statistically analyzed. Moreover, the roles of miR-99a, miR-99b, and miR-100 in regulating glioma cell migration and invasion were determined via transwell assay in vitro. RESULTS: Compared with non-neoplastic brain tissues, miR-99a, miR-99b, and miR-100 expression levels were all significantly decreased in glioma tissues (all P<0.001). miR-99a-low, miR-99b-low, and miR-100-low expression more frequently occurred in glioma patients with low Karnofsky performance score (<90) and high World Health Organization grade (III–IV). Further functional experiments revealed that the enforced expression of miR-99a, miR-99b, and miR-100 resulted in the inhibition of cellular migration and invasion in glioma cells. CONCLUSION: Our results strongly suggest that the aberrant expression of miR-99a, miR-99b, and miR-100 may be a common feature in human gliomas with aggressive clinicopathological features and may participate in malignant phenotypes of the tumors. These findings highlight the potential of the three miR-99 family members as novel therapeutic targets for human gliomas. Dove Medical Press 2016-06-20 /pmc/articles/PMC4920231/ /pubmed/27382299 http://dx.doi.org/10.2147/OTT.S99363 Text en © 2016 Zhang et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Zhang, Mingyu Guo, Yong Wu, Jun Chen, Fenghua Dai, Zhijie Fan, Shuangshi Li, Pengcheng Song, Tao Roles of microRNA-99 family in human glioma |
title | Roles of microRNA-99 family in human glioma |
title_full | Roles of microRNA-99 family in human glioma |
title_fullStr | Roles of microRNA-99 family in human glioma |
title_full_unstemmed | Roles of microRNA-99 family in human glioma |
title_short | Roles of microRNA-99 family in human glioma |
title_sort | roles of microrna-99 family in human glioma |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4920231/ https://www.ncbi.nlm.nih.gov/pubmed/27382299 http://dx.doi.org/10.2147/OTT.S99363 |
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