Bisphenol A induces focal adhesions assembly and activation of FAK, Src and ERK2 via GPER in MDA-MB-231 breast cancer cells

Bisphenol A (BPA) is an industrial synthetic chemical used in the production of polycarbonate plastics and epoxy resins. Human exposition to BPA is primarily through eating food, and drinking liquids, because BPA can leach from polycarbonate plastic containers, beverage cans and epoxy resins. BPA in...

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Veröffentlicht in:Toxicology in vitro 2020-08, Vol.66, p.104871, Article 104871
Hauptverfasser: Castillo-Sanchez, Rocio, Ramirez-Ricardo, Javier, Martinez-Baeza, Elia, Cortes-Reynosa, Pedro, Candanedo-Gonzales, Fernando, Gomez, Rocio, Salazar, Eduardo Perez
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container_start_page 104871
container_title Toxicology in vitro
container_volume 66
creator Castillo-Sanchez, Rocio
Ramirez-Ricardo, Javier
Martinez-Baeza, Elia
Cortes-Reynosa, Pedro
Candanedo-Gonzales, Fernando
Gomez, Rocio
Salazar, Eduardo Perez
description Bisphenol A (BPA) is an industrial synthetic chemical used in the production of polycarbonate plastics and epoxy resins. Human exposition to BPA is primarily through eating food, and drinking liquids, because BPA can leach from polycarbonate plastic containers, beverage cans and epoxy resins. BPA induces proliferation and migration in human breast cancer cells. The G protein-coupled estrogen receptor (GPER) is a G protein-coupled receptor coupled with Gs proteins that is activated by estrogen and estrogenic compounds and it is the receptor for BPA. However, the signal transduction pathways that mediate migration via BPA/GPER in triple negative breast cancer (TNBC) cells has not been studied in detail. Here, we demonstrate that BPA induces an increase of GPER expression and activation of FAK, Src and ERK2, and an increase of focal adhesion assembly via GPER in TNBC MDA-MB-231 cells. Moreover, BPA induces FAK and ERK2 activation, focal adhesion assembly and migration via epidermal growth factor receptor (EGFR) transactivation. Collectively our data showed that BPA via GPER and/or EGFR transactivation induces activation of signal transduction pathways that mediate migration in TNBC MDA-MB-231 cells. [Display omitted] •BPA induces migration via EGFR transactivation.•BPA induces FAK/ERK2 activation via GPER/EGFR transactivation.•BPA induces focal adhesion assembly via GPER/EGFR transactivation.
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Human exposition to BPA is primarily through eating food, and drinking liquids, because BPA can leach from polycarbonate plastic containers, beverage cans and epoxy resins. BPA induces proliferation and migration in human breast cancer cells. The G protein-coupled estrogen receptor (GPER) is a G protein-coupled receptor coupled with Gs proteins that is activated by estrogen and estrogenic compounds and it is the receptor for BPA. However, the signal transduction pathways that mediate migration via BPA/GPER in triple negative breast cancer (TNBC) cells has not been studied in detail. Here, we demonstrate that BPA induces an increase of GPER expression and activation of FAK, Src and ERK2, and an increase of focal adhesion assembly via GPER in TNBC MDA-MB-231 cells. Moreover, BPA induces FAK and ERK2 activation, focal adhesion assembly and migration via epidermal growth factor receptor (EGFR) transactivation. Collectively our data showed that BPA via GPER and/or EGFR transactivation induces activation of signal transduction pathways that mediate migration in TNBC MDA-MB-231 cells. 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Human exposition to BPA is primarily through eating food, and drinking liquids, because BPA can leach from polycarbonate plastic containers, beverage cans and epoxy resins. BPA induces proliferation and migration in human breast cancer cells. The G protein-coupled estrogen receptor (GPER) is a G protein-coupled receptor coupled with Gs proteins that is activated by estrogen and estrogenic compounds and it is the receptor for BPA. However, the signal transduction pathways that mediate migration via BPA/GPER in triple negative breast cancer (TNBC) cells has not been studied in detail. Here, we demonstrate that BPA induces an increase of GPER expression and activation of FAK, Src and ERK2, and an increase of focal adhesion assembly via GPER in TNBC MDA-MB-231 cells. Moreover, BPA induces FAK and ERK2 activation, focal adhesion assembly and migration via epidermal growth factor receptor (EGFR) transactivation. Collectively our data showed that BPA via GPER and/or EGFR transactivation induces activation of signal transduction pathways that mediate migration in TNBC MDA-MB-231 cells. [Display omitted] •BPA induces migration via EGFR transactivation.•BPA induces FAK/ERK2 activation via GPER/EGFR transactivation.•BPA induces focal adhesion assembly via GPER/EGFR transactivation.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>32325111</pmid><doi>10.1016/j.tiv.2020.104871</doi></addata></record>
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subjects Activation
Adhesion
Assembly
Benzhydryl Compounds - toxicity
Beverage cans
Bisphenol A
Breast cancer
Cell Line, Tumor
Cell Movement - drug effects
Cell proliferation
Containers
Epidermal growth factor
Epidermal growth factor receptors
Epoxy resins
Estrogens
Extracellular signal-regulated kinase
Focal adhesion
Focal adhesion kinase
Focal Adhesions - drug effects
GPER, FAK
Growth factors
Humans
Migration
Phenols - toxicity
Plasticizers - toxicity
Polycarbonate
Polycarbonate resins
Polymers
Protein-Tyrosine Kinases - metabolism
Proteins
Receptors
Receptors, Estrogen - genetics
Receptors, Estrogen - metabolism
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - metabolism
Signal transduction
Src
Src protein
Triple Negative Breast Neoplasms - metabolism
Xenoestrogens
title Bisphenol A induces focal adhesions assembly and activation of FAK, Src and ERK2 via GPER in MDA-MB-231 breast cancer cells
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