Relevance of CCL3/CCR5 axis in oral carcinogenesis

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dc.creatorJanine Mayra da Silva
dc.creatorAndréia Machado Leopoldino
dc.creatorRemo Castro Russo
dc.creatorTarcília Aparecida da Silva
dc.creatorTálita Pollyanna Moreira dos Santos
dc.creatorLays Martin Sobral
dc.creatorCelso Martins Queiroz-Junior
dc.creatorMilene Alvarenga Rachid
dc.creatorAmanda E.I. Proudfoot
dc.creatorGustavo Pompermaier Garlet
dc.creatorAline Carvalho Batista
dc.creatorMauro Martins Teixeira
dc.date.accessioned2025-06-23T21:28:53Z
dc.date.accessioned2025-09-09T00:09:51Z
dc.date.available2025-06-23T21:28:53Z
dc.date.issued2017
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/10.18632/oncotarget.16882
dc.identifier.issn1949-2553
dc.identifier.urihttps://hdl.handle.net/1843/83088
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofOncotarget
dc.rightsAcesso Aberto
dc.subjectChemokine CCL3
dc.subjectReceptors, CCR1
dc.subjectReceptors, CCR5
dc.subjectSquamous cell carcinoma of head and neck
dc.subjectChemokines
dc.subjectAngiogenesis
dc.subjectEvaluation study
dc.subjectEosinophils
dc.subjectCarcinogenesis
dc.subjectEpidermal Growth Factor
dc.subjectFibroblast Growth Factor 1
dc.subjectTransforming Growth Factor beta1
dc.subjectVascular Endothelial Growth Factor A
dc.subjectVascular Endothelial Growth Factor B
dc.subjectGenes
dc.subjectProteins
dc.subjectInterleukin-6
dc.subjectMatrix Metalloproteinase 2
dc.subjectMatrix Metalloproteinase 1
dc.subjectMatrix Metalloproteinase 8
dc.subjectMatrix Metalloproteinase 9
dc.subject.otherChemokines
dc.subject.otherCCL3
dc.subject.otherCCR1
dc.subject.otherCCR5
dc.subject.otherOSCC
dc.titleRelevance of CCL3/CCR5 axis in oral carcinogenesis
dc.typeArtigo de periódico
local.citation.epage51036
local.citation.spage51024
local.citation.volume8
local.description.resumoThe chemokine CCL3 is a chemotactic cytokine crucial for inflammatory cell recruitment in homeostatic and pathological conditions. CCL3 might stimulate cancer progression by promoting leukocyte accumulation, angiogenesis and tumour growth. The expression of CCL3 and its receptors CCR1 and CCR5 was demonstrated in oral squamous cell carcinoma (OSCC), but their role was not defined. Here, the functions of CCL3 were assessed using a model of chemically induced tongue carcinogenesis with 4-nitroquinoline-1-oxide (4NQO). Lineages of OSCC were used to analyse the effects of CCL3 in vitro. The 4NQO-induced lesions exhibited increased expression of CCL3, CCR1 and CCR5. CCL3-/- and CCR5-/- mice presented reduced incidence of tongue tumours compared to wild-type (WT) and CCR1-/- mice. Consistently, attenuated cytomorphological atypia and reduced cell proliferation were observed in lesions of CCL3-/- and CCR5-/- mice. OSCC from CCL3-/- mice exhibited lower infiltration of eosinophils and reduced expression of Egf, Fgf1, Tgf-β1, Vegfa, Vegfb, Itga-4, Vtn, Mmp-1a, Mmp-2 and Mmp-9 than WT mice. In vitro, CCL3 induced invasion and production of CCL5, IL-6, MMP -2, -8, -9. Blockage of CCL3 in vitro using α-CCL3 or Evasin-1 (a CCL3-binding protein) impaired tumour cell invasion. In conclusion, CCL3/CCR5 axis has pro-tumourigenic effects in oral carcinogenesis. The induction of inflammatory and angiogenic pathways and eosinophils recruitment appear to be the underlying mechanism explaining these effects. These data reveal potential protective effects of CCL3 blockade in oral cancer.
local.identifier.orcidhttps://orcid.org/0000-0002-1473-7455
local.identifier.orcidhttps://orcid.org/0000-0002-8313-4754
local.identifier.orcidhttps://orcid.org/0000-0002-1715-3834
local.identifier.orcidhttps://orcid.org/0000-0001-9623-7835
local.identifier.orcidhttps://orcid.org/0000-0002-9299-6858
local.identifier.orcidhttps://orcid.org/0000-0002-8731-850X
local.identifier.orcidhttps://orcid.org/0000-0002-7884-7709
local.identifier.orcidhttps://orcid.org/0000-0002-3142-6552
local.identifier.orcidhttps://orcid.org/0000-0002-4996-1860
local.identifier.orcidhttps://orcid.org/0000-0002-2117-5593
local.identifier.orcidhttps://orcid.org/0000-0002-6944-3008
local.publisher.countryBrasil
local.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICA
local.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA
local.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://www.oncotarget.com/article/16882/text/

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