A novel proteasome inhibitor acting in mitochondrial dysfunction, ER stress and ROS production

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dc.contributor.authorMaria, Durvanei Augusto
dc.contributor.authorSouza, Jean Gabriel de [UNIFESP]
dc.contributor.authorMorais, Katia Luciano Pereira [UNIFESP]
dc.contributor.authorBerra, Carolina Maria
dc.contributor.authorZampolli, Hamilton de Campos
dc.contributor.authorDemasi, Marilene
dc.contributor.authorSimons, Simone Michaela
dc.contributor.authorSaito, Renata de Freitas
dc.contributor.authorChammas, Roger
dc.contributor.authorChudzinski-Tavassi, Ana Marisa [UNIFESP]
dc.contributor.institutionInst Butantan
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.date.accessioned2016-01-24T14:31:48Z
dc.date.available2016-01-24T14:31:48Z
dc.date.issued2013-06-01
dc.description.abstractIn cancer-treatment, potentially therapeutic drugs trigger their effects through apoptotic mechanisms. Generally, cell response is manifested by Bcl-2 family protein regulation, the impairment of mitochondrial functions, and ROS production. Notwithstanding, several drugs operate through proteasome inhibition, which, by inducing the accumulation and aggregation of misfolded or unfolded proteins, can lead to endoplasmic reticulum (ER) stress. Accordingly, it was shown that Amblyomin-X, a Kunitz-type inhibitor identified in the transcriptome of the Amblyomma cajennense tick by ESTs sequence analysis of a cDNA library, obtained in recombinant protein form, induces apoptosis in murine renal adenocarcinoma (RENCA) cells by: inducing imbalance between pro- and anti-apoptotic Bcl-2 family proteins, dysfunction/mitochondrial damage, production of reactive oxygen species (ROS), caspase cascade activation, and proteasome inhibition, all ER-stress inductive. Moreover, there was no manifest action on normal mouse-fibroblast cells (NHI3T3), suggesting an Amblyomin-X tumor-cell selectivity. Taken together, these evidences indicate that Amblyomin-X could be a promising candidate for cancer therapy.en
dc.description.affiliationInst Butantan, Lab Bioquim & Biofis, BR-05503900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Bioquim, São Paulo, Brazil
dc.description.affiliationInst Butantan, Programa Posgrad Interunidades Biotecnol, USP, IPT, BR-05503900 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Fac Med, Lab Oncol Expt LIM24, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Bioquim, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipUniao Quimica Farmaceutica Nacional
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipIDFAPESP: FAPESP 2010/52669-3
dc.description.sponsorshipIDFAPESP: CAT/CEPID - 1998/14307-9
dc.format.extent493-505
dc.identifierhttp://dx.doi.org/10.1007/s10637-012-9871-1
dc.identifier.citationInvestigational New Drugs. Dordrecht: Springer, v. 31, n. 3, p. 493-505, 2013.
dc.identifier.doi10.1007/s10637-012-9871-1
dc.identifier.fileWOS000318657000001.pdf
dc.identifier.issn0167-6997
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/36357
dc.identifier.wosWOS:000318657000001
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofInvestigational New Drugs
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dc.subjectApoptosisen
dc.subjectBcl-2 family proteinen
dc.subjectCaspaseen
dc.subjectReactive oxygen speciesen
dc.subjectProteasomeen
dc.subjectEndoplasmic reticulum stressen
dc.subjectAmblyomin-Xen
dc.titleA novel proteasome inhibitor acting in mitochondrial dysfunction, ER stress and ROS productionen
dc.typeinfo:eu-repo/semantics/article
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