Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/34704
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dc.contributor.authorCalgarotto, Andrana K.
dc.contributor.authorSilva Pereira, Gustavo J. da [UNIFESP]
dc.contributor.authorBechara, Alexandre [UNIFESP]
dc.contributor.authorParedes-Gamero, Edgar J. [UNIFESP]
dc.contributor.authorBarbosa, Christiano M. V. [UNIFESP]
dc.contributor.authorHirata, Hanako [UNIFESP]
dc.contributor.authorSouza Queiroz, Mary L. de
dc.contributor.authorSmaili, Soraya Soubhi [UNIFESP]
dc.contributor.authorBincoletto, Claudia [UNIFESP]
dc.date.accessioned2016-01-24T14:26:58Z
dc.date.available2016-01-24T14:26:58Z
dc.date.issued2012-03-05
dc.identifierhttp://dx.doi.org/10.1016/j.ejphar.2011.12.031
dc.identifier.citationEuropean Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 678, n. 1-3, p. 6-14, 2012.
dc.identifier.issn0014-2999
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/34704
dc.description.abstractApoptosis induction is often associated with increased autophagy, indicating interplay between these two important cellular events in cell death and survival. in this study, the programmed cell death and autophagy induced by two nitrostyrene derivative compounds (NTS1 and NTS2) was studied using the tumorigenic Ehrlich ascitic tumor (EAT) cells. EAT cells were highly sensitive to NTS1 and NTS2 cytotoxicity in a dose-dependent manner. NTS1 and NTS2 IC50 was less than 15.0 mu M post 12 h incubation. Apoptosis was primarily induced by both compounds, as demonstrated by an increase in Annexin-V positive cells, concurrently with cytochrome c release from mitochondria to cytosol and caspase-3 activation. Although cytosolic Ca2+ mobilization is involved in autophagy as well as apoptosis in response to cellular stress in many cancer cell types, from the two nitrostyrene derivative compounds studied, mainly NTS1 mobilized this ion and disparate autophagy in EAT cells. These results suggest that EAT induced cell death by NTS1 and NTS2 involved a Ca2+-dependent and a Ca2+-independent pathways, respectively. in accordance with these results, the treatment of EAT cells with 3 methyladenine (3-MA), an autophagy inhibitor; significantly increased the number of apoptotic cells after NTS1 treatment, suggesting that pharmacological modulation of autophagy augments the NTS1 efficacy. Thus, we denote the importance of studies involving autophagy and apoptosis during pre-clinical studies of new drugs with anticancer properties. (C) 2011 Elsevier B. V. All rights reserved.en
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.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.format.extent6-14
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofEuropean Journal of Pharmacology
dc.rightsAcesso restrito
dc.subjectNitrostyrene derivative compoundsen
dc.subjectAutophagyen
dc.subjectCancer cellsen
dc.subjectApoptosisen
dc.subjectCalcium signalingen
dc.titleAutophagy inhibited Ehrlich ascitic tumor cells apoptosis induced by the nitrostyrene derivative compounds: Relationship with cytosolic calcium mobilizationen
dc.typeArtigo
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.description.affiliationUniversidade Federal de São Paulo UNIFESP, Escola Paulista Med, Dept Farmacol, São Paulo, Brazil
dc.description.affiliationUniv Estadual Campinas, UNICAMP, Dept Farmacol, FCM, Campinas, SP, Brazil
dc.description.affiliationUniversidade Federal de São Paulo UNIFESP, Escola Paulista Med, Dept Biofis, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo UNIFESP, Escola Paulista Med, Dept Farmacol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo UNIFESP, Escola Paulista Med, Dept Biofis, São Paulo, Brazil
dc.identifier.doi10.1016/j.ejphar.2011.12.031
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000300731400002
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Artigo

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