CHD7 promotes glioblastoma cell motility and invasiveness through transcriptional modulation of an invasion signature

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dc.contributorLaboratório de Biologia Molecularpt_BR
dc.contributorCentro de Excelência para Descoberta de Alvos Moleculares (CENTD)pt_BR
dc.contributor.authorMachado, Raquel A. C.pt_BR
dc.contributor.authorSchneider, Hannahpt_BR
dc.contributor.authorDe Ocesano-Pereira, Carlospt_BR
dc.contributor.authorLichtenstein, Flaviopt_BR
dc.contributor.authorAndrade, Fernandopt_BR
dc.contributor.authorFujita, Andrépt_BR
dc.contributor.authorTrombetta-Lima, Marinapt_BR
dc.contributor.authorWeller, Michaelpt_BR
dc.contributor.authorBowman-Colin, Christianpt_BR
dc.contributor.authorSogayar, Mari Cleidept_BR
dc.date.accessioned2020-07-09T21:23:06Z-
dc.date.available2020-07-09T21:23:06Z-
dc.date.issued2019-
dc.identifier.citationMachado RA.C., Schneider H, De Ocesano-Pereira C, Lichtenstein F, Andrade F, Fujita A, et al. CHD7 promotes glioblastoma cell motility and invasiveness through transcriptional modulation of an invasion signature. Sci Rep. 2019 Mar;9:3952. doi:10.1038/s41598-019-39564-w.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/2685-
dc.description.abstractChromatin remodeler proteins exert an important function in promoting dynamic modifications in the chromatin architecture, performing a central role in regulating gene transcription. Deregulation of these molecular machines may lead to striking perturbations in normal cell function. The CHD7 gene is a member of the chromodomain helicase DNA-binding family and, when mutated, has been shown to be the cause of the CHARGE syndrome, a severe developmental human disorder. Moreover, CHD7 has been described to be essential for neural stem cells and it is also highly expressed or mutated in a number of human cancers. However, its potential role in glioblastoma has not yet been tested. Here, we show that CHD7 is up-regulated in human glioma tissues and we demonstrate that CHD7 knockout (KO) in LN-229 glioblastoma cells suppresses anchorage-independent growth and spheroid invasion in vitro. Additionally, CHD7 KO impairs tumor growth and increases overall survival in an orthotopic mouse xenograft model. Conversely, ectopic overexpression of CHD7 in LN-428 and A172 glioblastoma cell lines increases cell motility and invasiveness in vitro and promotes LN-428 tumor growth in vivo. Finally, RNA-seq analysis revealed that CHD7 modulates a specific transcriptional signature of invasion-related target genes. Further studies should explore clinical-translational implications for glioblastoma treatment.pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorshipFinanciadora de Estudos e Projetos (FINEP)pt_BR
dc.description.sponsorshipBanco Nacional de Desenvolvimento Econômico e Social (BNDES)pt_BR
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt_BR
dc.format.extent3952pt_BR
dc.languageengpt_BR
dc.relation.ispartofScientific Reportspt_BR
dc.rightsOpen Accesspt_BR
dc.titleCHD7 promotes glioblastoma cell motility and invasiveness through transcriptional modulation of an invasion signaturept_BR
dc.typeArticlept_BR
dc.identifier.doi10.1038/s41598-019-39564-wpt_BR
dc.identifier.urlhttps://doi.org/10.1038/s41598-019-39564-wpt_BR
dc.contributor.externalUniversidade de São Paulo (USP)¦¦Brasilpt_BR
dc.contributor.externalUniversity of Zurich¦¦Alemanhapt_BR
dc.contributor.externalHarvard University¦¦Estados Unidospt_BR
dc.identifier.citationvolume9pt_BR
dc.relation.ispartofabbreviatedSci Reppt_BR
dc.identifier.citationabntv. 9, 3952, mar. 2019pt_BR
dc.identifier.citationvancouver2019 Mar;9:3952pt_BR
dc.contributor.butantanLichtenstein, Flavio|:Aluno|:Centro de Excelência para Descoberta de Alvos Moleculares (CENTD):Laboratório de Biologia Molecular|:pt_BR
dc.sponsorship.butantanBanco Nacional de Desenvolvimento Econômico e Social (BNDES)¦¦09.2.1066.1pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦148684/2013-0pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦401430/2013-8pt_BR
dc.sponsorship.butantanConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)¦¦457601/2013-2pt_BR
dc.sponsorship.butantanCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)¦¦AUX-PE PROBITEC 908/2012pt_BR
dc.sponsorship.butantanFinanciadora de Estudos e Projetos (FINEP)¦¦01.06.0664.00pt_BR
dc.sponsorship.butantanFinanciadora de Estudos e Projetos (FINEP)¦¦01.08.0622.00pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2013/23271-0pt_BR
dc.sponsorship.butantanFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)¦¦2014/21614-0pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
item.openairetypeArticle-
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