Bisphenol A disruption promotes mammary tumor microenvironment via phenotypic cell polarization and inflammatory response

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dc.contributor.authorRuiz, Thalles F. R. [UNESP]
dc.contributor.authorColleta, Simone J. [UNESP]
dc.contributor.authordos Santos, Diego D. [UNESP]
dc.contributor.authorCastro, Nayara F. C. [UNESP]
dc.contributor.authorCabral, Ágata S. [UNESP]
dc.contributor.authorCalmon, Marilia F. [UNESP]
dc.contributor.authorRahal, Paula [UNESP]
dc.contributor.authorGil, Cristiane D. [UNESP]
dc.contributor.authorGirol, Ana Paula
dc.contributor.authorVilamaior, Patricia S. L. [UNESP]
dc.contributor.authorLeonel, Ellen C. R.
dc.contributor.authorTaboga, Sebastião R. [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversity Center Padre Albino (UNIFIPA)
dc.contributor.institutionUniversidade Federal de Goiás (UFG)
dc.date.accessioned2023-07-29T16:09:11Z
dc.date.available2023-07-29T16:09:11Z
dc.date.issued2023-06-01
dc.description.abstractInflammation in the established tumor microenvironment (TME) is often associated with a poor prognosis of breast cancer. Bisphenol A (BPA) is an endocrine-disrupting chemical that acts as inflammatory promoter and tumoral facilitator in mammary tissue. Previous studies demonstrated the onset of mammary carcinogenesis at aging when BPA exposure occurred in windows of development/susceptibility. We aim to investigate the inflammatory repercussions of BPA in TME in mammary gland (MG) during neoplastic development in aging. Female Mongolian gerbils were exposed to low (50 µg/kg) or high BPA (5000 µg/kg) doses during pregnancy and lactation. They were euthanized at 18 months of age (aging) and the MG were collected for inflammatory markers and histopathological analysis. Contrarily to control MG, BPA induced carcinogenic development mediated by COX-2 and p-STAT3 expression. BPA was also able to promote macrophage and mast cell (MC) polarization in tumoral phenotype, evidenced by pathways for recruitment and activation of these inflammatory cells and tissue invasiveness triggered by tumor necrosis factor-alpha and transforming growth factor-beta 1 (TGF-β1). Increase of tumor-associated macrophages, M1 (CD68 + iNOS+) and M2 (CD163+) expressing pro-tumoral mediators and metalloproteases was observed; this aspect greatly contributed to stromal remodeling and invasion of neoplastic cells. In addition, the MC population drastically increased in BPA-exposed MG. Tryptase-positive MCs increased in disrupted MG and expressed TGF-β1, contributing to EMT process during carcinogenesis mediated by BPA. BPA exposure interfered in inflammatory response by releasing and enhancing the expression of mediators that contribute to tumor growth and recruitment of inflammatory cells that promote a malignant profile.en
dc.description.affiliationDepartment of Biological Sciences Institute of Biosciences Humanities and Exact Sciences São Paulo State University (UNESP), São Paulo
dc.description.affiliationDepartment of Morphology and Genetics Paulista School of Medicine Federal University of São Paulo (UNIFESP), São Paulo
dc.description.affiliationLaboratory of Genomic Studies São Paulo State University, São Paulo
dc.description.affiliationDepartment of Basics Sciences University Center Padre Albino (UNIFIPA), São Paulo
dc.description.affiliationDepartment of Histology Embryology and Cell Biology Institute of Biological Sciences (ICB III) Federal University of Goiás (UFG), Goiás
dc.description.affiliationUnespDepartment of Biological Sciences Institute of Biosciences Humanities and Exact Sciences São Paulo State University (UNESP), São Paulo
dc.description.affiliationUnespLaboratory of Genomic Studies São Paulo State University, São Paulo
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIdFAPESP: 18/23383-6
dc.description.sponsorshipIdFAPESP: 20/00160-1
dc.description.sponsorshipIdFAPESP: 20/01240-9
dc.description.sponsorshipIdCNPq: 302938/2020-6
dc.format.extent1136-1146
dc.identifierhttp://dx.doi.org/10.1002/cbin.12007
dc.identifier.citationCell Biology International, v. 47, n. 6, p. 1136-1146, 2023.
dc.identifier.doi10.1002/cbin.12007
dc.identifier.issn1095-8355
dc.identifier.issn1065-6995
dc.identifier.scopus2-s2.0-85150655125
dc.identifier.urihttp://hdl.handle.net/11449/249786
dc.language.isoeng
dc.relation.ispartofCell Biology International
dc.sourceScopus
dc.subjectbisphenol A
dc.subjectmast cells
dc.subjectTGF-β1
dc.subjectTNF-α
dc.subjecttumor-associated macrophages
dc.titleBisphenol A disruption promotes mammary tumor microenvironment via phenotypic cell polarization and inflammatory responseen
dc.typeArtigo
unesp.author.orcid0000-0002-8760-8945[9]
unesp.author.orcid0000-0001-9559-5497[10]
unesp.author.orcid0000-0002-4597-3346[11]
unesp.author.orcid0000-0002-0970-4288[12]

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