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Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells
Many kinds of endocrine-disrupting chemicals (EDCs), for example, the environmental estrogens bisphenol A and nonylphenol, may regulate the activity of estrogen receptor α (ERα) and therefore induce potential disruption of normal endocrine function. However, the involvement of EDCs in human cancers,...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove Medical Press
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913548/ https://www.ncbi.nlm.nih.gov/pubmed/27366082 http://dx.doi.org/10.2147/OTT.S105745 |
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author | Ma, Hongda Yao, Yao Wang, Changli Zhang, Liyu Cheng, Long Wang, Yiren Wang, Tao Liang, Erguang Jia, Hui Ye, Qinong Hou, Mingxiao Feng, Fan |
author_facet | Ma, Hongda Yao, Yao Wang, Changli Zhang, Liyu Cheng, Long Wang, Yiren Wang, Tao Liang, Erguang Jia, Hui Ye, Qinong Hou, Mingxiao Feng, Fan |
author_sort | Ma, Hongda |
collection | PubMed |
description | Many kinds of endocrine-disrupting chemicals (EDCs), for example, the environmental estrogens bisphenol A and nonylphenol, may regulate the activity of estrogen receptor α (ERα) and therefore induce potential disruption of normal endocrine function. However, the involvement of EDCs in human cancers, especially in endocrine-related cancer neuroblastoma regulation, is not very clear. In this work, results showed that upon bisphenol A or nonylphenol treatment, the transcription factor activity of ERα was significantly increased in neuroblastoma cell line SH-SY5Y. Bisphenol A and nonylphenol could enhance ERα activity via recruiting it to the target gene promoter. Furthermore, treatment of bisphenol A and nonylphenol enhanced the in vitro proliferation, invasion, and migration ability of neuroblastoma cells. By investigating the role of EDC-induced ERα upregulation, our data extend the understanding of the function of EDCs and further suggest that ERα might be a potential therapeutic target in human neuroblastoma treatment. |
format | Online Article Text |
id | pubmed-4913548 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-49135482016-06-30 Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells Ma, Hongda Yao, Yao Wang, Changli Zhang, Liyu Cheng, Long Wang, Yiren Wang, Tao Liang, Erguang Jia, Hui Ye, Qinong Hou, Mingxiao Feng, Fan Onco Targets Ther Original Research Many kinds of endocrine-disrupting chemicals (EDCs), for example, the environmental estrogens bisphenol A and nonylphenol, may regulate the activity of estrogen receptor α (ERα) and therefore induce potential disruption of normal endocrine function. However, the involvement of EDCs in human cancers, especially in endocrine-related cancer neuroblastoma regulation, is not very clear. In this work, results showed that upon bisphenol A or nonylphenol treatment, the transcription factor activity of ERα was significantly increased in neuroblastoma cell line SH-SY5Y. Bisphenol A and nonylphenol could enhance ERα activity via recruiting it to the target gene promoter. Furthermore, treatment of bisphenol A and nonylphenol enhanced the in vitro proliferation, invasion, and migration ability of neuroblastoma cells. By investigating the role of EDC-induced ERα upregulation, our data extend the understanding of the function of EDCs and further suggest that ERα might be a potential therapeutic target in human neuroblastoma treatment. Dove Medical Press 2016-06-13 /pmc/articles/PMC4913548/ /pubmed/27366082 http://dx.doi.org/10.2147/OTT.S105745 Text en © 2016 Ma 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 Ma, Hongda Yao, Yao Wang, Changli Zhang, Liyu Cheng, Long Wang, Yiren Wang, Tao Liang, Erguang Jia, Hui Ye, Qinong Hou, Mingxiao Feng, Fan Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells |
title | Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells |
title_full | Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells |
title_fullStr | Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells |
title_full_unstemmed | Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells |
title_short | Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells |
title_sort | transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol a treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913548/ https://www.ncbi.nlm.nih.gov/pubmed/27366082 http://dx.doi.org/10.2147/OTT.S105745 |
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