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Long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro

Extensive use of triclosan (2,4,4′‐trichloro‐2′‐hydroxydiphenyl ether) as an antimicrobial agent in household and personal care products has resulted in global exposure of the human population. Its presence in human tissues, including milk, and its oestrogen‐disrupting properties raise concerns for...

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Autores principales: Farasani, Abdullah, Darbre, Philippa D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8246770/
https://www.ncbi.nlm.nih.gov/pubmed/33171535
http://dx.doi.org/10.1002/jat.4097
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author Farasani, Abdullah
Darbre, Philippa D.
author_facet Farasani, Abdullah
Darbre, Philippa D.
author_sort Farasani, Abdullah
collection PubMed
description Extensive use of triclosan (2,4,4′‐trichloro‐2′‐hydroxydiphenyl ether) as an antimicrobial agent in household and personal care products has resulted in global exposure of the human population. Its presence in human tissues, including milk, and its oestrogen‐disrupting properties raise concerns for an involvement in breast cancer. Because metastatic tumour spread is the main cause of breast cancer mortality, we have investigated the effects of triclosan on cell migration and invasion using three human breast epithelial cell lines and using concentrations comparable with those in human tissues. Long‐term exposure to 10(−7) M of triclosan resulted in increased migration and invasion as measured by xCELLigence technology for all three cell lines, for the immortalized but nontransformed MCF‐10F breast epithelial cells (after 28 weeks), the oestrogen‐responsive MCF‐7 breast cancer cells (after 17 weeks) and the oestrogen‐unresponsive MDA‐MB‐231 breast cancer cells (after 20 weeks). The effects were therefore not limited to cancerous cells or to oestrogen‐responsive cells. This was paralleled in the MCF‐10F and MCF‐7 (but not MDA‐MB‐231) cells by a reduction in levels of E‐cadherin mRNA as measured by reverse transcription–polymerase chain reaction (RT‐PCR) and of E‐cadherin protein as measured by western immunoblotting, suggesting a mechanism involving epithelial‐to‐mesenchymal transition. This adds triclosan to the increasing list of ingredients of personal care products that can not only enter human breast tissue and increase cell proliferation but also influence cell motility. If mixtures of components in household and personal care products contribute to increasing cell migration and invasion, then reduction in exposure could offer a strategy for reducing breast cancer spread.
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spelling pubmed-82467702021-07-02 Long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro Farasani, Abdullah Darbre, Philippa D. J Appl Toxicol Research Articles Extensive use of triclosan (2,4,4′‐trichloro‐2′‐hydroxydiphenyl ether) as an antimicrobial agent in household and personal care products has resulted in global exposure of the human population. Its presence in human tissues, including milk, and its oestrogen‐disrupting properties raise concerns for an involvement in breast cancer. Because metastatic tumour spread is the main cause of breast cancer mortality, we have investigated the effects of triclosan on cell migration and invasion using three human breast epithelial cell lines and using concentrations comparable with those in human tissues. Long‐term exposure to 10(−7) M of triclosan resulted in increased migration and invasion as measured by xCELLigence technology for all three cell lines, for the immortalized but nontransformed MCF‐10F breast epithelial cells (after 28 weeks), the oestrogen‐responsive MCF‐7 breast cancer cells (after 17 weeks) and the oestrogen‐unresponsive MDA‐MB‐231 breast cancer cells (after 20 weeks). The effects were therefore not limited to cancerous cells or to oestrogen‐responsive cells. This was paralleled in the MCF‐10F and MCF‐7 (but not MDA‐MB‐231) cells by a reduction in levels of E‐cadherin mRNA as measured by reverse transcription–polymerase chain reaction (RT‐PCR) and of E‐cadherin protein as measured by western immunoblotting, suggesting a mechanism involving epithelial‐to‐mesenchymal transition. This adds triclosan to the increasing list of ingredients of personal care products that can not only enter human breast tissue and increase cell proliferation but also influence cell motility. If mixtures of components in household and personal care products contribute to increasing cell migration and invasion, then reduction in exposure could offer a strategy for reducing breast cancer spread. John Wiley and Sons Inc. 2020-11-10 2021-07 /pmc/articles/PMC8246770/ /pubmed/33171535 http://dx.doi.org/10.1002/jat.4097 Text en © 2020 The Authors. Journal of Applied Toxicology published by John Wiley & Sons Ltd https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Farasani, Abdullah
Darbre, Philippa D.
Long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro
title Long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro
title_full Long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro
title_fullStr Long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro
title_full_unstemmed Long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro
title_short Long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro
title_sort long‐term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8246770/
https://www.ncbi.nlm.nih.gov/pubmed/33171535
http://dx.doi.org/10.1002/jat.4097
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