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MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition
Docetaxel is commonly used as an effective chemotherapeutic agent in breast cancer treatment, but the underlying mechanisms of drug resistance are not fully understood. The purpose of this study was to investigate the possible role of miR-129-3p in breast cancer cell resistance to docetaxel. MiR-129...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4614026/ https://www.ncbi.nlm.nih.gov/pubmed/26487539 http://dx.doi.org/10.1038/srep15424 |
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author | Zhang, Yuan Wang, Yu Wei, Yifang Li, Mengyang Yu, Shentong Ye, Mingxiang Zhang, Hongmei Chen, Suning Liu, Wenchao Zhang, Jian |
author_facet | Zhang, Yuan Wang, Yu Wei, Yifang Li, Mengyang Yu, Shentong Ye, Mingxiang Zhang, Hongmei Chen, Suning Liu, Wenchao Zhang, Jian |
author_sort | Zhang, Yuan |
collection | PubMed |
description | Docetaxel is commonly used as an effective chemotherapeutic agent in breast cancer treatment, but the underlying mechanisms of drug resistance are not fully understood. The purpose of this study was to investigate the possible role of miR-129-3p in breast cancer cell resistance to docetaxel. MiR-129 and miR-129-3p inhibitor were transfected into breast cancer cells to investigate their effects on chemoresistance to docetaxel. The function of miR-129-3p was evaluated by apoptosis, cell proliferation, and cell cycle assays. We found that miR-129-3p was up-regulated in MDA-MB-231/Doc cells, concurrent with CP110 down-regulation, compared to the parental MDA-MB-231 cells. In vitro drug sensitivity assays demonstrated that miR-129-3p inhibition sensitized MDA-MB-231/Doc and MCF-7 cells to docetaxel, whereas miR-129 overexpression enhanced MDA-MB-231 and MCF-7 cell resistance to docetaxel. Ectopic miR-129 expression reduced CP110 expression and the luciferase activity of a CP110 3′ untranslated region-based reporter construct in MDA-MB-231 cells, suggesting that CP110 is a direct miR-129-3p target. We demonstrated that restoration of CP110 expression in MDA-MB-231 and MCF-7 cells by miR-129 overexpression rendered the cells sensitive to docetaxel. In a nude xenograft model, miR-129 up-regulation significantly decreased MDA-MB-231 cells’ response to docetaxel. Our findings suggest that miR-129-3p down-regulation potentially sensitizes breast cancer cells to docetaxel treatment. |
format | Online Article Text |
id | pubmed-4614026 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-46140262015-10-29 MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition Zhang, Yuan Wang, Yu Wei, Yifang Li, Mengyang Yu, Shentong Ye, Mingxiang Zhang, Hongmei Chen, Suning Liu, Wenchao Zhang, Jian Sci Rep Article Docetaxel is commonly used as an effective chemotherapeutic agent in breast cancer treatment, but the underlying mechanisms of drug resistance are not fully understood. The purpose of this study was to investigate the possible role of miR-129-3p in breast cancer cell resistance to docetaxel. MiR-129 and miR-129-3p inhibitor were transfected into breast cancer cells to investigate their effects on chemoresistance to docetaxel. The function of miR-129-3p was evaluated by apoptosis, cell proliferation, and cell cycle assays. We found that miR-129-3p was up-regulated in MDA-MB-231/Doc cells, concurrent with CP110 down-regulation, compared to the parental MDA-MB-231 cells. In vitro drug sensitivity assays demonstrated that miR-129-3p inhibition sensitized MDA-MB-231/Doc and MCF-7 cells to docetaxel, whereas miR-129 overexpression enhanced MDA-MB-231 and MCF-7 cell resistance to docetaxel. Ectopic miR-129 expression reduced CP110 expression and the luciferase activity of a CP110 3′ untranslated region-based reporter construct in MDA-MB-231 cells, suggesting that CP110 is a direct miR-129-3p target. We demonstrated that restoration of CP110 expression in MDA-MB-231 and MCF-7 cells by miR-129 overexpression rendered the cells sensitive to docetaxel. In a nude xenograft model, miR-129 up-regulation significantly decreased MDA-MB-231 cells’ response to docetaxel. Our findings suggest that miR-129-3p down-regulation potentially sensitizes breast cancer cells to docetaxel treatment. Nature Publishing Group 2015-10-21 /pmc/articles/PMC4614026/ /pubmed/26487539 http://dx.doi.org/10.1038/srep15424 Text en Copyright © 2015, Macmillan Publishers Limited 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 Zhang, Yuan Wang, Yu Wei, Yifang Li, Mengyang Yu, Shentong Ye, Mingxiang Zhang, Hongmei Chen, Suning Liu, Wenchao Zhang, Jian MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition |
title | MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition |
title_full | MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition |
title_fullStr | MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition |
title_full_unstemmed | MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition |
title_short | MiR-129-3p promotes docetaxel resistance of breast cancer cells via CP110 inhibition |
title_sort | mir-129-3p promotes docetaxel resistance of breast cancer cells via cp110 inhibition |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4614026/ https://www.ncbi.nlm.nih.gov/pubmed/26487539 http://dx.doi.org/10.1038/srep15424 |
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