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Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer

miR-145 has been implicated in the progression of breast cancer. Here, we report that its expression is decreased in breast cancer specimens and cell lines and that this low level of expression is associated with DNA methylation of its gene, MIR145. Methylation of MIR145 has previously been correlat...

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Autores principales: Liu, Shui-Yi, Li, Xiao-Yi, Chen, Wei-Qun, Hu, Hui, Luo, Bo, Shi, Yu-Xiang, Wu, Tang-Wei, Li, Yong, Kong, Qing-Zhi, Lu, Hong-Da, Lu, Zhong-Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617460/
https://www.ncbi.nlm.nih.gov/pubmed/28977900
http://dx.doi.org/10.18632/oncotarget.18686
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author Liu, Shui-Yi
Li, Xiao-Yi
Chen, Wei-Qun
Hu, Hui
Luo, Bo
Shi, Yu-Xiang
Wu, Tang-Wei
Li, Yong
Kong, Qing-Zhi
Lu, Hong-Da
Lu, Zhong-Xin
author_facet Liu, Shui-Yi
Li, Xiao-Yi
Chen, Wei-Qun
Hu, Hui
Luo, Bo
Shi, Yu-Xiang
Wu, Tang-Wei
Li, Yong
Kong, Qing-Zhi
Lu, Hong-Da
Lu, Zhong-Xin
author_sort Liu, Shui-Yi
collection PubMed
description miR-145 has been implicated in the progression of breast cancer. Here, we report that its expression is decreased in breast cancer specimens and cell lines and that this low level of expression is associated with DNA methylation of its gene, MIR145. Methylation of MIR145 has previously been correlated with cell migration and invasion, both in vivo and in vitro. We found that demethylation of MIR145 reactivates miR-145 and contributes to the anti-cancer properties of 5-aza-2′-deoxyazacytidine (5-AzaC). Therefore, miR-145 is a potentially valuable biomarker for breast cancer.
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spelling pubmed-56174602017-10-03 Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer Liu, Shui-Yi Li, Xiao-Yi Chen, Wei-Qun Hu, Hui Luo, Bo Shi, Yu-Xiang Wu, Tang-Wei Li, Yong Kong, Qing-Zhi Lu, Hong-Da Lu, Zhong-Xin Oncotarget Research Paper miR-145 has been implicated in the progression of breast cancer. Here, we report that its expression is decreased in breast cancer specimens and cell lines and that this low level of expression is associated with DNA methylation of its gene, MIR145. Methylation of MIR145 has previously been correlated with cell migration and invasion, both in vivo and in vitro. We found that demethylation of MIR145 reactivates miR-145 and contributes to the anti-cancer properties of 5-aza-2′-deoxyazacytidine (5-AzaC). Therefore, miR-145 is a potentially valuable biomarker for breast cancer. Impact Journals LLC 2017-06-27 /pmc/articles/PMC5617460/ /pubmed/28977900 http://dx.doi.org/10.18632/oncotarget.18686 Text en Copyright: © 2017 Liu et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Liu, Shui-Yi
Li, Xiao-Yi
Chen, Wei-Qun
Hu, Hui
Luo, Bo
Shi, Yu-Xiang
Wu, Tang-Wei
Li, Yong
Kong, Qing-Zhi
Lu, Hong-Da
Lu, Zhong-Xin
Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer
title Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer
title_full Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer
title_fullStr Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer
title_full_unstemmed Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer
title_short Demethylation of the MIR145 promoter suppresses migration and invasion in breast cancer
title_sort demethylation of the mir145 promoter suppresses migration and invasion in breast cancer
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617460/
https://www.ncbi.nlm.nih.gov/pubmed/28977900
http://dx.doi.org/10.18632/oncotarget.18686
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