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dc.typeArtigo de periódicopt_BR
dc.titleKnocking Down Low Molecular Weight Protein Tyrosine Phosphatase (lmw-ptp) Reverts Chemoresistance Through Inactivation Of Src And Bcr-abl Proteins.pt_BR
dc.contributor.authorFerreira, Paula Apt_BR
dc.contributor.authorRuela-de-Sousa, Roberta Rpt_BR
dc.contributor.authorQueiroz, Karla C Spt_BR
dc.contributor.authorSouza, Ana Carolina Spt_BR
dc.contributor.authorMilani, Renatopt_BR
dc.contributor.authorPilli, Ronaldo Aloisept_BR
dc.contributor.authorPeppelenbosch, Maikel Ppt_BR
dc.contributor.authorden Hertog, Jeroenpt_BR
dc.contributor.authorFerreira, Carmen Vpt_BR
unicamp.authorPaula A Ferreira, Laboratory of Bioassays and Signal Transduction, Biochemistry Department, Biology Institute, University of Campinas (UNICAMP), Campinas, São Paulo, Brazil.pt_BR R Ruela-de-Sousa,pt C S Queiroz,pt Carolina S Souza,pt Milani,pt Aloise Pilli,pt P Peppelenbosch,pt den Hertog,pt V Ferreira,pt
dc.subjectAntineoplastic Agentspt_BR
dc.subjectCaspase 3pt_BR
dc.subjectCell Line, Tumorpt_BR
dc.subjectCell Survivalpt_BR
dc.subjectDrug Resistance, Neoplasmpt_BR
dc.subjectFusion Proteins, Bcr-ablpt_BR
dc.subjectGene Expression Regulation, Leukemicpt_BR
dc.subjectK562 Cellspt_BR
dc.subjectMolecular Weightpt_BR
dc.subjectProtein Tyrosine Phosphatasespt_BR
dc.subjectSrc-family Kinasespt_BR
dc.description.abstractThe development of multidrug resistance (MDR) limits the efficacy of continuous chemotherapeutic treatment in chronic myelogenous leukemia (CML). Low molecular weight protein tyrosine phosphatase (LMW-PTP) is up-regulated in several cancers and has been associated to poor prognosis. This prompted us to investigate the involvement of LMW-PTP in MDR. In this study, we investigated the role of LMW-PTP in a chemoresistant CML cell line, Lucena-1. Our results showed that LMW-PTP is highly expressed and 7-fold more active in Lucena-1 cells compared to K562 cells, the non-resistant cell line. Knocking down LMW-PTP in Lucena-1 cells reverted chemoresistance to vincristine and imatinib mesylate, followed by a decrease of Src and Bcr-Abl phosphorylation at the activating sites, inactivating both kinases. On the other hand, overexpression of LMW-PTP in K562 cells led to chemoresistance to vincristine. Our findings describe, for the first time, that LMW-PTP cooperates with MDR phenotype, at least in part, through maintaining Src and Bcr-Abl kinases in more active statuses. These findings suggest that inhibition of LMW-PTP may be a useful strategy for the development of therapies for multidrug resistant CML.en
dc.relation.ispartofPlos Onept_BR
dc.relation.ispartofabbreviationPLoS ONEpt_BR
dc.identifier.citationPlos One. v. 7, n. 9, p. e44312, 2012.pt_BR
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