Crosstalk between B16 melanoma cells and B-1 lymphocytes induces global changes in tumor cell gene expression

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dc.contributor.authorXander, Patricia [UNIFESP]
dc.contributor.authorNovaes e Brito, Ronni Romulo
dc.contributor.authorPerez, Elizabeth Cristina
dc.contributor.authorPozzibon, Jaqueline Maciel [UNIFESP]
dc.contributor.authorSouza, Camila Ferreira de [UNIFESP]
dc.contributor.authorPellegrino, Renata [UNIFESP]
dc.contributor.authorBernardo, Viviane [UNIFESP]
dc.contributor.authorJasiulionis, Miriam Galvonas [UNIFESP]
dc.contributor.authorMariano, Mario [UNIFESP]
dc.contributor.authorLopes, Jose Daniel [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionCtr Univ Sao Camilo
dc.date.accessioned2016-01-24T14:34:31Z
dc.date.available2016-01-24T14:34:31Z
dc.date.issued2013-10-01
dc.description.abstractThe analysis of gene expression patterns in cancers has improved the understanding of the mechanisms underlying the process of metastatic progression. However, the acquisition of invasive behavior in melanoma is poorly understood. in melanoma, components of the immune system can contribute to tumor progression, and inflammatory cells can influence almost all aspects of cancer progression, including metastasis. Recent studies have attributed an important role to B-1 cells, a subset of B lymphocytes, in melanoma progression. in vitro interactions between B16 melanoma cells and B-1 lymphocytes lead to increased B16 cell metastatic potential, but the molecular changes induced by B-1 lymphocytes on B16 cells have not yet been elucidated. in this study, we used a microarray approach to assess the gene expression profile of B16 melanoma cells following contact with B-1 lymphocytes (B16B1). the microarray analysis identified upregulation in genes involved with metastatic progression, such as ctss, ccl5, cxcl2 and stat3. RT-qPCR confirmed this increase in mRNA expression in B16B1 samples. As previous studies have indicated that the ERK1/2 MAPK cascade is activated in melanoma cells following contact with B-1 lymphocytes, RT-qPCR was performed with RNA from melanoma cells before and after contacting B-1 cells and untreated or treated with ERK phosphorylation inhibitors. the results showed that the expression of stat3, ctss and cxcl2 increased in B16B1 but decreased following ERK1/2 MAPK inhibition. Ccl5 gene expression increased after contacting B-1 cells and was maintained at the same level following inhibitor treatment. Stat3 was verified and validated at the protein level by Western blot analysis. STAT3 expression was also significantly increased in B16B1, suggesting that this pathway can also contribute to the increased metastatic phenotype observed in our model. These results indicated that B-1 cells induce important global gene expression changes in B16 melanoma cells. We also evaluated the relationship of some of the genes identified as differentially expressed and the ERK1/2 MAPK cascade. This work may have important implications for understanding the role of B-1 lymphocytes and the ERK/MAPK cascade in the metastatic process. (C) 2013 Elsevier GmbH. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Ciencias Biol, Campus Diadema, Brazil
dc.description.affiliationCtr Univ Sao Camilo, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Microbiol Imunol & Parasitol, BR-04023900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Farmacol, BR-04023900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Psicobiol, BR-04023900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Informat Saude, BR-04023900 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Ciencias Biol, Campus Diadema, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Microbiol Imunol & Parasitol, BR-04023900 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Farmacol, BR-04023900 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Psicobiol, BR-04023900 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Informat Saude, BR-04023900 São Paulo, Brazil
dc.description.sourceWeb of Science
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: 2007/51501-9
dc.description.sponsorshipIDFAPESP: 2007/50521-6
dc.description.sponsorshipIDCNPq: 502452/2008-0
dc.format.extent1293-1303
dc.identifierhttp://dx.doi.org/10.1016/j.imbio.2013.04.017
dc.identifier.citationImmunobiology. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 218, n. 10, p. 1293-1303, 2013.
dc.identifier.doi10.1016/j.imbio.2013.04.017
dc.identifier.issn0171-2985
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/36820
dc.identifier.wosWOS:000323588900009
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofImmunobiology
dc.rightsAcesso restrito
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectB-1 cellsen
dc.subjectMelanomaen
dc.subjectMicroarrayen
dc.subjectGene expressionen
dc.subjectMetastasesen
dc.titleCrosstalk between B16 melanoma cells and B-1 lymphocytes induces global changes in tumor cell gene expressionen
dc.typeArtigo
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