Role of atypical chemokine receptor ACKR2 in experimental oral squamous cell carcinogenesis

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dc.creatorJanine Mayra da Silva
dc.creatorTálita Pollyanna Moreira dos Santos
dc.creatorAdriana Machado Saraiva
dc.creatorAna Laura Fernandes de Oliveira
dc.creatorGustavo Pompermaier Garlet
dc.creatorAline Carvalho Batista
dc.creatorRicardo Alves de Mesquita
dc.creatorRemo Castro Russo
dc.creatorTarcília Aparecida da Silva
dc.date.accessioned2025-04-23T21:10:57Z
dc.date.accessioned2025-09-08T23:30:24Z
dc.date.available2025-04-23T21:10:57Z
dc.date.issued2019-06
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.1016/j.cyto.2018.03.001
dc.identifier.issn1096-0023
dc.identifier.urihttps://hdl.handle.net/1843/81795
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofCytokine
dc.rightsAcesso Restrito
dc.subjectChemokines
dc.subjectReceptors, chemokine
dc.subjectChemokine receptor D6
dc.subjectInflammation
dc.subjectCarcinogenesis
dc.subjectChemokine CCL2
dc.subjectInterleukin-6
dc.subjectInterleukin-17
dc.subjectCarcinoma, squamous cell
dc.subjectAngiogenesis
dc.subjectRNA, messenger
dc.subjectCell adhesion molecules
dc.subjectExtracellular matrix
dc.subject.otherChemokines
dc.subject.otherOSCC
dc.subject.otherACKR2
dc.subject.otherD6
dc.titleRole of atypical chemokine receptor ACKR2 in experimental oral squamous cell carcinogenesis
dc.typeArtigo de periódico
local.citation.epage167
local.citation.spage160
local.citation.volume118
local.description.resumoBackground: Chemokines and chemokine receptors are critical in oral tumourigenesis. The atypical chemokine receptor ACKR2 is a scavenger of CC chemokines controlling the availability of these molecules at tumour sites, but the role of ACKR2 in the context of oral carcinogenesis is unexplored. Methods: In this study, wild-type (WT) and ACKR2 deficient mice (ACKR2-/-) were treated with chemical carcinogen 4-nitroquinoline-1-oxide (4NQO) for induction of oral carcinogenesis. Tongues were collected for macro and microscopic analysis and to evaluate the expression of ACKRs, CC chemokines and its receptors, inflammatory cytokines, angiogenic factors, adhesion molecules and extracellular matrix components. Results: An increased expression of ACKR2 in squamous cell carcinoma (SCC) lesions of 4NQO-treated WT mice was observed. No significant differences were seen in the ACKR1, ACKR3 and ACKR4 mRNA expression comparing SCC lesions from WT and ACKR2-/- treated mice. Significantly higher expression of CCL2, IL-6 and IL-17 was detected in ACKR2-/- treated mice. In contrast, the expression of other CC-chemokines, and receptors, angiogenic factors, adhesion molecules and extracellular matrix components were similarly increased in SCC lesions of both groups. Clinical and histopathological analysis revealed no differences in inflammatory cell recruitment and in the SCC incidence comparing WT and ACKR2-/- treated mice. Conclusion: The results suggest that ACKR2 expression regulates inflammation in tumour-microenvironment but the absence of ACKR2 does not impact chemically-induced oral carcinogenesis.
local.identifier.orcidhttps://orcid.org/0000-0002-1473-7455
local.identifier.orcidhttps://orcid.org/0000-0002-9299-6858
local.identifier.orcidhttps://orcid.org/0000-0002-5071-8382
local.identifier.orcidhttps://orcid.org/0000-0002-2117-5593
local.identifier.orcidhttps://orcid.org/0000-0003-3207-4007
local.identifier.orcidhttps://orcid.org/0000-0002-1715-3834
local.identifier.orcidhttps://orcid.org/0000-0001-9623-7835
local.publisher.countryBrasil
local.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICA
local.publisher.departmentICB - DEPARTAMENTO DE MICROBIOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://www.sciencedirect.com/science/article/pii/S1043466618300772?via%3Dihub

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