Combined p19Arf and interferon-beta gene transfer enhances cell death of B16 melanoma in vitro and in vivo

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorMERKEL, C. A.
dc.contributor.authorMEDRANO, R. F. V.
dc.contributor.authorBARAUNA, V. G.
dc.contributor.authorSTRAUSS, B. E.
dc.date.accessioned2013-09-23T16:55:57Z
dc.date.available2013-09-23T16:55:57Z
dc.date.issued2013
dc.description.abstractApproximately 90% of melanomas retain wild-type p53, a characteristic that may help shape the development of novel treatment strategies. Here, we employed an adenoviral vector where transgene expression is,controlled by p53 to deliver the p19 alternate reading frame (An) and interferon-beta (IFN beta) complementary DNAs in the B16 mouse model of melanoma. In vitro, cell death was enhanced by combined gene transfer (63.82 +/- 15.30% sub-GO cells); yet introduction of a single gene resulted in significantly fewer hypoploid cells (37.73 +/- 7.3% or 36.96 +/- 11.58%, p19Arf or IFN beta, respectively, P < 0.05). Annexin V staining and caspase-3 cleavage indicate a cell death mechanism consistent with apoptosis. Using reverse transcriptase quantitative PCR, we show that key transcriptional targets of p53 were upregulated in the presence of p19Arf, although treatment with IFN beta did not alter expression of the genes studied. In situ gene therapy revealed significant inhibition of subcutaneous tumors by IFN beta (571 +/- 25 mm(3)) or the combination of p19Arf and IFN beta (489 +/- 124 mm(3)) as compared with the LacZ control (1875 +/- 33 mm(3), P < 0.001); whereas p19Arf yielded an intermediate result (1053 +/- 169 mm(3), P < 0.01 vs control). However, only the combination was associated with increased cell death and prolonged survival (P < 0.01). As shown here, the combined transfer of p19Arf and IFN beta using p53-responsive vectors enhanced cell death both in vitro and in vivo.
dc.description.indexMEDLINE
dc.description.sponsorshipFAPESP (Fundacao de Amparo Pesquisa do Estado de Sao Paulo) [06/57823-5, 2010/03958-2, 07/50210-0, 11/50911-0]
dc.identifier.citationCANCER GENE THERAPY, v.20, n.5, p.317-325, 2013
dc.identifier.doi10.1038/cgt.2013.23
dc.identifier.issn0929-1903
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/2462
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUP
dc.relation.ispartofCancer Gene Therapy
dc.rightsrestrictedAccess
dc.rights.holderCopyright NATURE PUBLISHING GROUP
dc.subjectp53
dc.subjectp14Arf/p19Arf
dc.subjectinterferon
dc.subjectmelanoma
dc.subjectadenovirus
dc.subjectcell death
dc.subject.otheradvanced malignant-melanoma
dc.subject.otherifn-beta
dc.subject.otheradenoviral vector
dc.subject.otherantiviral defense
dc.subject.othertumor suppression
dc.subject.otherstabilizes p53
dc.subject.otherphase-ii
dc.subject.othertherapy
dc.subject.othermurine
dc.subject.otherexpression
dc.subject.wosBiotechnology & Applied Microbiology
dc.subject.wosOncology
dc.subject.wosGenetics & Heredity
dc.subject.wosMedicine, Research & Experimental
dc.titleCombined p19Arf and interferon-beta gene transfer enhances cell death of B16 melanoma in vitro and in vivo
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.citation.scopus21
hcfmusp.contributor.author-fmusphcCHRISTIAN ALBERT MERKEL
hcfmusp.contributor.author-fmusphcRUAN FELIPE VIEIRA MEDRANO
hcfmusp.contributor.author-fmusphcVALERIO GARRONE BARAUNA
hcfmusp.contributor.author-fmusphcBRYAN ERIC STRAUSS
hcfmusp.description.beginpage317
hcfmusp.description.endpage325
hcfmusp.description.issue5
hcfmusp.description.volume2013
hcfmusp.origemWOS
hcfmusp.origem.pubmed23618951
hcfmusp.origem.scopus2-s2.0-84878019926
hcfmusp.origem.wosWOS:000319031400007
hcfmusp.publisher.cityLONDON
hcfmusp.publisher.countryENGLAND
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