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miR-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7
MicroRNAs (miRNAs) play important roles in diverse biological processes and are emerging as key regulators of tumorigenesis and tumor progression. Among the differentially expressed miRNAs in breast cancer, miR-125b was revealed to be deregulated and associated with poor prognosis and chemoresistanc...
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/PMC4863692/ https://www.ncbi.nlm.nih.gov/pubmed/27226726 http://dx.doi.org/10.2147/OTT.S102713 |
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author | Hong, Liquan Pan, Feng Jiang, Huifen Zhang, Lahong Liu, Yuhua Cai, Chengsong Hua, Chunzhen Luo, Xian Sun, Jinhua Chen, Zhaojun |
author_facet | Hong, Liquan Pan, Feng Jiang, Huifen Zhang, Lahong Liu, Yuhua Cai, Chengsong Hua, Chunzhen Luo, Xian Sun, Jinhua Chen, Zhaojun |
author_sort | Hong, Liquan |
collection | PubMed |
description | MicroRNAs (miRNAs) play important roles in diverse biological processes and are emerging as key regulators of tumorigenesis and tumor progression. Among the differentially expressed miRNAs in breast cancer, miR-125b was revealed to be deregulated and associated with poor prognosis and chemoresistance in triple-negative breast cancer (TNBC), but the mechanism is still unknown. In our study, we showed downregulated expression of miR-125b in TNBC tissues and decreased migration and invasion in miR-125b-expressing Hs578T cells. MAP2K7 was then detected to be a novel target of miR-125b, and downregulation of MAP2K7 by miR-125b was similar to transient knockdown of MAP2K7 which hindered epithelial–mesenchymal transition (EMT) of Hs578T cells. Upregulation of MAP2K7 in miR-125b-overexpressing Hs578T cells partly rescued the migration and invasion suppression of miR-125b. Furthermore, MAP2K7 was overexpressed in TNBC samples compared with normal tissues and negatively correlated with miR-125b expression. In light of these findings, miR-125b emerged as a tumor suppressor in TNBC by targeting MAP2K7 to inhibit EMT. |
format | Online Article Text |
id | pubmed-4863692 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-48636922016-05-25 miR-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7 Hong, Liquan Pan, Feng Jiang, Huifen Zhang, Lahong Liu, Yuhua Cai, Chengsong Hua, Chunzhen Luo, Xian Sun, Jinhua Chen, Zhaojun Onco Targets Ther Original Research MicroRNAs (miRNAs) play important roles in diverse biological processes and are emerging as key regulators of tumorigenesis and tumor progression. Among the differentially expressed miRNAs in breast cancer, miR-125b was revealed to be deregulated and associated with poor prognosis and chemoresistance in triple-negative breast cancer (TNBC), but the mechanism is still unknown. In our study, we showed downregulated expression of miR-125b in TNBC tissues and decreased migration and invasion in miR-125b-expressing Hs578T cells. MAP2K7 was then detected to be a novel target of miR-125b, and downregulation of MAP2K7 by miR-125b was similar to transient knockdown of MAP2K7 which hindered epithelial–mesenchymal transition (EMT) of Hs578T cells. Upregulation of MAP2K7 in miR-125b-overexpressing Hs578T cells partly rescued the migration and invasion suppression of miR-125b. Furthermore, MAP2K7 was overexpressed in TNBC samples compared with normal tissues and negatively correlated with miR-125b expression. In light of these findings, miR-125b emerged as a tumor suppressor in TNBC by targeting MAP2K7 to inhibit EMT. Dove Medical Press 2016-05-04 /pmc/articles/PMC4863692/ /pubmed/27226726 http://dx.doi.org/10.2147/OTT.S102713 Text en © 2016 Hong 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 Hong, Liquan Pan, Feng Jiang, Huifen Zhang, Lahong Liu, Yuhua Cai, Chengsong Hua, Chunzhen Luo, Xian Sun, Jinhua Chen, Zhaojun miR-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7 |
title | miR-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7 |
title_full | miR-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7 |
title_fullStr | miR-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7 |
title_full_unstemmed | miR-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7 |
title_short | miR-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7 |
title_sort | mir-125b inhibited epithelial–mesenchymal transition of triple-negative breast cancer by targeting map2k7 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4863692/ https://www.ncbi.nlm.nih.gov/pubmed/27226726 http://dx.doi.org/10.2147/OTT.S102713 |
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