FGF2 antiproliferative stimulation induces proteomic dynamic changes and high expression of FOSB and JUNB in K-ras-driven mouse tumor cells

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dc.contributorLCC - Laboratório de Ciclo Celularpt_BR
dc.contributorLETA - Laboratório de Toxinologia Aplicadapt_BR
dc.contributor.authorVitorino, Francisca Nathália de Lunapt_BR
dc.contributor.authorMontoni, Fabiopt_BR
dc.contributor.authorMoreno, Jaqueline Nevespt_BR
dc.contributor.authorSouza, Bruno Ferreira dept_BR
dc.contributor.authorLopes, Mariana de Camargopt_BR
dc.contributor.authorCordeiro, Barbarapt_BR
dc.contributor.authorFonseca, Cecília Sellapt_BR
dc.contributor.authorGilmore, Joshua M.pt_BR
dc.contributor.authorSardiu, Mihaela I.pt_BR
dc.contributor.authorReis, Marcelo da Silvapt_BR
dc.contributor.authorFlorens, Laurence A.pt_BR
dc.contributor.authorWashburn, Michael P.pt_BR
dc.contributor.authorArmelin, Hugo Aguirrept_BR
dc.contributor.authorda Cunha, Julia Pinheiro Chagaspt_BR
dc.date.accessioned2020-07-09T21:22:40Z-
dc.date.available2020-07-09T21:22:40Z-
dc.date.issued2018pt_BR
dc.identifier.citationVitorino FNL, Montoni F, Moreno JN, Souza BF, Lopes MC, Cordeiro B, et al. FGF2 antiproliferative stimulation induces proteomic dynamic changes and high expression of FOSB and JUNB in K-ras-driven mouse tumor cells. Proteomics. 2018 Jul;18(17):1800203. doi:10.1002/pmic.201800203.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/2657-
dc.description.abstractFibroblast growth factor 2 (FGF2) is a well-known cell proliferation promoter; however, it can also induce cell cycle arrest. To gain insight into the molecular mechanisms of this antiproliferative effect, for the first time, the early systemic proteomic differences induced by this growth factor in a K-Ras-driven mouse tumor cell line using a quantitative proteomics approach are investigated. More than 2900 proteins are quantified, indicating that terms associated with metabolism, RNA processing, replication, and transcription are enriched among proteins differentially expressed upon FGF2 stimulation. Proteomic trend dynamics indicate that, for proteins mainly associated with DNA replication and carbohydrate metabolism, an FGF2 stimulus delays their abundance changes, whereas FGF2 stimulation accelerates other metabolic programs. Transcription regulatory network analysis indicates master regulators of FGF2 stimulation, including two critical transcription factors, FOSB and JUNB. Their expression dynamics, both in the Y1 cell line (a murine model of adenocarcinoma cells) and in two other human cell lines (SK-N-MC and UM-UC-3) also susceptible to FGF2 antiproliferative effects, are investigated. Both protein expression levels depend on fibroblast growth factor receptor (FGFR) and src signaling. JUNB and FOSB knockdown do not rescue cells from the growth arrest induced by FGF2; however, FOSB knockdown rescue cells from DNA replication delay, indicating that FOSB expression underlies one of the FGF2 antiproliferative effects, namely, S-phase progression delay.pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt_BR
dc.description.sponsorshipStowers Institute for Medical Researchpt_BR
dc.format.extent1800203pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofProteomicspt_BR
dc.titleFGF2 antiproliferative stimulation induces proteomic dynamic changes and high expression of FOSB and JUNB in K-ras-driven mouse tumor cellspt_BR
dc.typeArticlept_BR
dc.identifier.doi10.1002/pmic.201800203pt_BR
dc.identifier.urlhttp://dx.doi.org/10.1002/pmic.201800203pt_BR
dc.contributor.externalUniversidade de São Paulo (USP)¦¦Brasilpt_BR
dc.contributor.externalStowers Institute for Medical Research¦¦Estados Unidospt_BR
dc.contributor.externalUniversity of Kansas Medical Center¦¦Estados Unidospt_BR
dc.identifier.citationvolume18pt_BR
dc.identifier.citationissue17pt_BR
dc.subject.keywordantiproliferativept_BR
dc.subject.keywordDNA replicationpt_BR
dc.subject.keywordFGF2pt_BR
dc.subject.keywordFOSBpt_BR
dc.subject.keywordJUNBpt_BR
dc.subject.keywordproteomicspt_BR
dc.subject.keywordsrcpt_BR
dc.relation.ispartofabbreviatedProteomicspt_BR
dc.identifier.citationabntv. 18, n. 17, 18002013, jul. 2018pt_BR
dc.identifier.citationvancouver2018 Jul;18(17):1800203pt_BR
dc.contributor.butantanMoreno, Jaqueline Neves|:Aluno|:LCC - Laboratório de Ciclo Celular|:pt_BR
dc.contributor.butantanLopes, Mariana de Camargo|:Aluno|:LCC - Laboratório de Ciclo Celular|:pt_BR
dc.contributor.butantanCordeiro, Barbara|:Aluno|:LCC - Laboratório de Ciclo Celular|:pt_BR
dc.contributor.butantanFonseca, Cecília Sella|:Aluno|:LCC - Laboratório de Ciclo Celular|:pt_BR
dc.contributor.butantanReis, Marcelo da Silva|:Pesquisador|:LCC - Laboratório de Ciclo Celular|:pt_BR
dc.contributor.butantanArmelin, Hugo Aguirre|:Pesquisador|:LCC - Laboratório de Ciclo Celular|:pt_BR
dc.contributor.butantanda Cunha, Julia Pinheiro Chagas|:Pesquisador|:LCC - Laboratório de Ciclo Celular|:pt_BR
dc.contributor.butantanVitorino, Francisca Nathália de Luna|:Aluno|:LCC - Laboratório de Ciclo Celular|:PrimeiroAutorpt_BR
dc.contributor.butantanMontoni, Fábio|:Aluno PPGTOX|:LCC - Laboratório de Ciclo Celular:Laboratório Especial de Toxinologia Aplicada (LETA)|:pt_BR
dc.contributor.butantanSouza, Bruno Ferreira de|:Aluno|:Laboratório Especial de Toxinologia Aplicada (LETA):LCC - Laboratório de Ciclo Celular|:pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦pt_BR
dc.sponsorship.butantanCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)¦¦pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦11/22619-7pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦13/07467-1pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2015-10037-4pt_BR
dc.sponsorship.butantanStowers Institute for Medical Research¦¦pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
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