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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/67847
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dc.creatorTatiana Fernandes Araujo Almeidapt_BR
dc.creatorSicília Rezende Oliveirapt_BR
dc.creatorJanine Mayra da Silvapt_BR
dc.creatorAna Laura Fernandes de Oliveirapt_BR
dc.creatorZenilda de Lourdes Cardealpt_BR
dc.creatorHelvécio Costa Menezespt_BR
dc.creatorJosé Messias Gomespt_BR
dc.creatorGabriel Henrique Campolina silvapt_BR
dc.creatorCleida Aparecida Oliveirapt_BR
dc.creatorSoraia Macaript_BR
dc.creatorGustavo Pompermaier Garletpt_BR
dc.creatorIvana Márcia Alves Dinizpt_BR
dc.creatorAndréia Machado Leopoldinopt_BR
dc.creatorTarcília Aparecida Silvapt_BR
dc.date.accessioned2024-04-29T14:55:48Z-
dc.date.available2024-04-29T14:55:48Z-
dc.date.issued2021-
dc.citation.volume286pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.envpol.2021.117296pt_BR
dc.identifier.issn1873-6424pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/67847-
dc.description.resumoBisphenol A (BPA) is an endocrine disrupting chemical able to promote hormone-responsive tumors. The major route of BPA contamination being oral, the aim of the present study was to investigate BPA effects on oral cells. Here, we evaluated the impact of sub-chronic in vivo exposure to BPA and its in vitro effects on neoplastic and non-neoplastic oral cells. We evaluated the oral mucosa of mice chronically exposed to BPA (200 mg/L). The response of keratinocytes (NOK–SI) and Head and Neck (HN) Squamous Cell Carcinoma (SCC), HN12 and HN13 cell lines to BPA was examined. In vivo, BPA accumulated in oral tissues and caused an increase in epithelial proliferative activity. BPA disrupted the function of keratinocytes by altering pro-survival and proliferative pathways and the secretion of cytokines and growth factors. In tumor cells, BPA induced proliferative, invasive, pro-angiogenic, and epigenetic paths. Our data highlight the harmful effects of BPA on oral mucosa and, tumorigenic and non-tumorigenic cells. Additionally, BPA may be a modifier of oral cancer cell behavior by prompting a functional shift to a more aggressive phenotype.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.description.sponsorshipFAPESP - Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentFAO - DEPARTAMENTO DE ODONTOLOGIA RESTAURADORApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIApt_BR
dc.publisher.departmentICX - DEPARTAMENTO DE QUÍMICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofEnvironmental Pollutionpt_BR
dc.rightsAcesso Restritopt_BR
dc.subjectBisphenol Apt_BR
dc.subjectMouth neoplasmspt_BR
dc.subjectCell culture techniquespt_BR
dc.subjectHistone acetylationpt_BR
dc.subjectEstrogenpt_BR
dc.subject.otherCelulas - Cultura e meios de cultura.pt_BR
dc.subject.otherTumorespt_BR
dc.subject.otherEstrogenospt_BR
dc.titleEffects of high-dose bisphenol a on the mouse oral mucosa: a possible link with oral cancerspt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.sciencedirect.com/science/article/pii/S0269749121008782pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-3216-5649pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-8164-2122pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1473-7455pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1383-6299pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5759-612Xpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-9610-7846pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-7643-6589pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5071-8382pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-4261-0037pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-8313-4754pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-9623-7835pt_BR
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