Bisphenol a exposure promotes the migration of NCM460 cells via estrogen receptor‐mediated integrin β1/MMP‐9 pathway

Shi, Tonglin; Zhao, Chao; Li, Zhuoyu; Zhang, Quanbin; Jin, Xiaoting

doi:10.1002/tox.22090

Cited by 22 publications

(21 citation statements)

References 37 publications

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“…Our present study revealed that BPA can trigger the in vitro cell motility of TNBC cells, which is consistent with recent data that BPA can stimulate the cell migration in some hormone‐dependent or hormone‐independent cancers . Furthermore, our study indicated that nanomolar BPA can increase the expression and transcription of MMP‐2 and MMP‐9 in TNBC cells in a time‐dependent manner.…”

Section: Discussioncontrasting

confidence: 41%

“…Our results that BPA can up‐regulate the expression of MMP‐2 and MMP‐9 in TNBC cells are consistent with recent data observed in ovarian and lung cancer cells. Other studies also demonstrated that BPA stimulates MMP‐9 secretion by human granulosa lutein cells and normal colon epithelial cells (NCM460 cells) . BPA can also increase the expression of Vim and FN in colorectal and cervical cancer cells but not in the present study by the use of MDA‐MB‐231 or BT‐549 cells.…”

Section: Discussionmentioning

confidence: 99%

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Bisphenol A Increases the Migration and Invasion of Triple‐Negative Breast Cancer Cells via Oestrogen‐related Receptor Gamma

Zhang

Liu

Weng

et al. 2016

Basic Clin Pharma Tox

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Triple-negative breast cancer (TNBC) is characterized by great metastasis and invasion capability. Our study revealed that nanomolar bisphenol A (BPA), one of the most ubiquitous endocrine disruptors, can increase wound closure and invasion of both MDA-MB-231 and BT-549 cells. BPA treatment can increase protein and mRNA expression of matrix metalloproteinase-2 (MMP-2) and MMP-9, while had no effect on the expression of vimentin (Vim) and fibronectin (FN) in TNBC cells. The expression of G-protein-coupled receptor (GPER), which has been suggested to mediate rapid oestrogenic signals, was not varied in BPA-treated MDA-MB-231 and BT-549 cells. Its inhibitor G15 also had no effect on BPA-induced MMPs expression and cell invasion. Interestingly, BPA treatment can significantly increase the mRNA and protein expressions of oestrogen-related receptor γ (ERRγ), but not ERRα or ERRβ, in both MDA-MB-231 and BT-549 cells. The knock-down of ERRγ can markedly attenuate BPA-induced expression of MMP-2 and MMP-9 in TNBC cells. BPA treatment can activate both ERK1/2 and Akt in TNBC cells. Both inhibitors of ERK1/2 (PD98059) and Akt (LY294002) can attenuate BPA-induced ERRγ expression and cell invasion of MDA-MB-231 cells. Collectively, our data revealed that BPA can increase the expression of MMPs and in vitro motility of TNBC cells via ERRγ. Both activation of ERK1/2 and Akt participated in this process. Our study suggests that more attention should be paid to the roles of xenoestrogens such as BPA in the development and progression of TNBC.

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Section: Discussioncontrasting

confidence: 41%

Section: Discussionmentioning

confidence: 99%

Bisphenol A Increases the Migration and Invasion of Triple‐Negative Breast Cancer Cells via Oestrogen‐related Receptor Gamma

Zhang

Liu

Weng

et al. 2016

Basic Clin Pharma Tox

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“…21,25 Furthermore, BPA treatment can also increase the expression of matrix metalloproteinases in cancer cells. 10,21,26 The effects of BPA on the expression and activation of these signal molecules required further studies.…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A regulates Snail‐mediated epithelial‐mesenchymal transition in hemangioma cells

Zhai¹,

Jiang²,

Li³

et al. 2016

Cell Biochemistry & Function

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Hemangioma (HA) can be exposed to bisphenol A (BPA) through direct skin absorption. Although numerous studies indicated that BPA can trigger the progression of cancers, there is no study concerning the effects of BPA on development of HA. Our present study revealed that nanomolar BPA can significantly increase the in vitro migration and invasion of HA cells via induction of epithelial-mesenchymal transition (EMT), which was evidenced by the upregulation of vimentin and downregulation of E-cadherin. The BPA treatment also significantly increased the expression and nuclear localization of Snail and the key transcription factor of EMT, while it had no effect on the expression of other transcription factors such as Slug, Twist, or ZEB1. Silencing of Snail by small interfering RNAs attenuated BPA-induced downregulation of cadherin and upregulation of vimentin, suggesting that Snail is essential for BPA-induced EMT. Both estrogen receptor α (ERα) and G protein-coupled estrogen receptor (GPER) were expressed in HA cells; furthermore, BPA treatment can increase the expression of both ERα and GPER. However, only the inhibitor of ERα (ICI 182, 780), and not GPER (G15), can abolish BPA-induced upregulation of Snail. It suggested that ERα is involved in BPA-induced EMT of HA cells. Collectively, our data suggested that BPA can trigger the EMT of HA cells via ERα/Snail signals. It indicated that more attention should be paid to the skin exposure to BPA for HA patients.

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“…La senescencia del endotelio tras la exposición al BPA se tradujo en un empeoramiento de la capacidad de reparar una herida en la monocapa de células. Algunos estudios [35] realizaron ensayos de herida en células epiteliales de mucosa de colon NCM460, mostrando que a dosis similares a las nuestras no se inducía la reparación de la herida, sin embargo, en fibroblastos cardiacos con otras concentraciones más altas (10 M) y en tratamientos a 24 y 48 horas se encontró el efecto contrario [36]. Hay que resaltar que los tratamientos es estos estudios son modelos agudos y el nuestro es un modelo de exposición a cinco días por lo que no son totalmente comparables.…”

Section: Discussionunclassified

Bisfenol A induce la senescencia en células del endotelio aórtico de ratón

Porcel¹,

Redondo²

2019

DIANAS

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Palabras clave: Bisfenol A; senescencia; ateroesclerosis; envejecimiento; endotelio ResumenEl Bisfenol A (BPA) es un compuesto fenólico, al que estamos expuestos en nuestro día a día, debido a su alta presencia en envases y otros productos. Muchos estudios habían señalado ya a este compuesto como disruptor endocrino. En este estudio nos plantemos su papel en la senescencia de células de endotelio vascular debido a la relación existente entre el BPA y la ateroesclerosis ya indicada por estudios previos. Ya se había observado que a altas dosis el BPA producía la muerte celular, pero los resultados obtenidos determinan que a bajas dosis el BPA (10 nM) y en un tiempo de cinco días, produce senescencia en células de endotelio cardíaco murino determinado por cambios morfológicos en las células, aumento de la actividad -Gal, y de la expresión de P53 y p16. Además, el BPA induce un fenotipo secretor asociado a la senescencia, generando un mayor número de microvesículas que tienen un efecto en la migración celular. Además, mediante ensayos de herida se demuestra un retardo en la migración celular a causa del BPA, así como una disminución de la producción de óxido nítrico. En conclusión, se ha determinado que el BPA a una concentración considerada como segura produce senescencia en las células del endotelio de ratón acompañado de disfunción del endotelio. Cita: Rodrigo Porcel, Alfonso; Saura Redondo, Marta (2019) Bisfenol A induce la senescencia en células del endotelio aórtico de ratón. dianas 8 (2): e201909fa01. ISSN 1886-8746 (electronic) journal.dianas.e201909fa01 Copyright: © Rodrigo-Porcel A, Saura-Redondo M. Algunos derechos reservados. Este es un artículo openaccess distribuido bajo los términos de una licencia de Creative Commons Reconocimiento-NoComercial-SinObraDerivada 4.0 Internacional. http://creativecommons.org/licenses/by-nc-nd/4.0/

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Bisphenol a exposure promotes the migration of NCM460 cells via estrogen receptor‐mediated integrin β1/MMP‐9 pathway

Cited by 22 publications

References 37 publications

Bisphenol A Increases the Migration and Invasion of Triple‐Negative Breast Cancer Cells via Oestrogen‐related Receptor Gamma

Bisphenol A Increases the Migration and Invasion of Triple‐Negative Breast Cancer Cells via Oestrogen‐related Receptor Gamma

Bisphenol A regulates Snail‐mediated epithelial‐mesenchymal transition in hemangioma cells

Bisfenol A induce la senescencia en células del endotelio aórtico de ratón

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