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Bioinformatics identification of dysregulated microRNAs in triple negative breast cancer based on microRNA expression profiling
Triple negative breast cancer (TNBC) accounts for approximately 15–20% of all breast cancer cases and is usually more aggressive with a poorer clinical outcome compared with other breast cancer subtypes. Evidence of the involvement of microRNAs (miRNAs) in cancer has provided an opportunity for the...
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/PMC5778821/ https://www.ncbi.nlm.nih.gov/pubmed/29435032 http://dx.doi.org/10.3892/ol.2017.7707 |
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author | Chen, Junqing Chen, Zhanhong Huang, Jian Chen, Feng Ye, Weiwu Ding, Guojun Wang, Xiaojia |
author_facet | Chen, Junqing Chen, Zhanhong Huang, Jian Chen, Feng Ye, Weiwu Ding, Guojun Wang, Xiaojia |
author_sort | Chen, Junqing |
collection | PubMed |
description | Triple negative breast cancer (TNBC) accounts for approximately 15–20% of all breast cancer cases and is usually more aggressive with a poorer clinical outcome compared with other breast cancer subtypes. Evidence of the involvement of microRNAs (miRNAs) in cancer has provided an opportunity for the development of novel effective therapeutic targets in TNBC. In the present study, the miRNA expression profiles of the human breast cancer cell line, MDA-MB-231, and MCF-7 cells, was evaluated by using miRNA microarray analysis. A total of 107 differentially expressed miRNAs (57 upregulated and 50 downregulated) were identified in MDA-MB-231 cells compared with MCF-7 cells. Five prominently dysregulated miRNAs (miR-200c-3p, miR-221-3p, miR-222-3p, miR-192-5p and miR-146a) were further confirmed by reverse transcription-quantitative polymerase chain reaction. In addition, gene ontology analysis and pathway enrichment analysis revealed that the dysregulated miRNAs and predicted targets were found to be involved in the mitogen-activated protein kinase, Wnt, and transforming growth factor-β signaling pathways, which were known to contribute to TNBC progression and metastasis. Finally, miRNA gene network analyses suggested that miR-200c may serve as a crucial miRNA in breast cancer. Taken together, these findings may provide a comprehensive view of the function of aberrant miRNAs involved in TNBC, and dysregulated miRNAs hold promise as potential biomarkers and therapeutic targets for patients with TNBC. |
format | Online Article Text |
id | pubmed-5778821 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57788212018-02-12 Bioinformatics identification of dysregulated microRNAs in triple negative breast cancer based on microRNA expression profiling Chen, Junqing Chen, Zhanhong Huang, Jian Chen, Feng Ye, Weiwu Ding, Guojun Wang, Xiaojia Oncol Lett Articles Triple negative breast cancer (TNBC) accounts for approximately 15–20% of all breast cancer cases and is usually more aggressive with a poorer clinical outcome compared with other breast cancer subtypes. Evidence of the involvement of microRNAs (miRNAs) in cancer has provided an opportunity for the development of novel effective therapeutic targets in TNBC. In the present study, the miRNA expression profiles of the human breast cancer cell line, MDA-MB-231, and MCF-7 cells, was evaluated by using miRNA microarray analysis. A total of 107 differentially expressed miRNAs (57 upregulated and 50 downregulated) were identified in MDA-MB-231 cells compared with MCF-7 cells. Five prominently dysregulated miRNAs (miR-200c-3p, miR-221-3p, miR-222-3p, miR-192-5p and miR-146a) were further confirmed by reverse transcription-quantitative polymerase chain reaction. In addition, gene ontology analysis and pathway enrichment analysis revealed that the dysregulated miRNAs and predicted targets were found to be involved in the mitogen-activated protein kinase, Wnt, and transforming growth factor-β signaling pathways, which were known to contribute to TNBC progression and metastasis. Finally, miRNA gene network analyses suggested that miR-200c may serve as a crucial miRNA in breast cancer. Taken together, these findings may provide a comprehensive view of the function of aberrant miRNAs involved in TNBC, and dysregulated miRNAs hold promise as potential biomarkers and therapeutic targets for patients with TNBC. D.A. Spandidos 2018-03 2017-12-28 /pmc/articles/PMC5778821/ /pubmed/29435032 http://dx.doi.org/10.3892/ol.2017.7707 Text en Copyright: © Chen 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 Chen, Junqing Chen, Zhanhong Huang, Jian Chen, Feng Ye, Weiwu Ding, Guojun Wang, Xiaojia Bioinformatics identification of dysregulated microRNAs in triple negative breast cancer based on microRNA expression profiling |
title | Bioinformatics identification of dysregulated microRNAs in triple negative breast cancer based on microRNA expression profiling |
title_full | Bioinformatics identification of dysregulated microRNAs in triple negative breast cancer based on microRNA expression profiling |
title_fullStr | Bioinformatics identification of dysregulated microRNAs in triple negative breast cancer based on microRNA expression profiling |
title_full_unstemmed | Bioinformatics identification of dysregulated microRNAs in triple negative breast cancer based on microRNA expression profiling |
title_short | Bioinformatics identification of dysregulated microRNAs in triple negative breast cancer based on microRNA expression profiling |
title_sort | bioinformatics identification of dysregulated micrornas in triple negative breast cancer based on microrna expression profiling |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5778821/ https://www.ncbi.nlm.nih.gov/pubmed/29435032 http://dx.doi.org/10.3892/ol.2017.7707 |
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