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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.authorVIEIRA, Igor de Luna
dc.contributor.authorTAMURA, Rodrigo Esaki
dc.contributor.authorHUNGER, Aline
dc.contributor.authorSTRAUSS, Bryan E.
dc.date.accessioned2019-05-30T13:42:46Z
dc.date.available2019-05-30T13:42:46Z
dc.date.issued2019
dc.identifier.citationJOURNAL OF INTERFERON AND CYTOKINE RESEARCH, v.39, n.4, p.246-258, 2019
dc.identifier.issn1079-9907
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/31888
dc.description.abstractTumor vasculature plays a central role in tumor progression, making it an attractive therapeutic target. In this study, we explore the antiangiogenic potential of our melanoma gene therapy approach combining interferon beta (IFN beta) and p19Arf gene transfer. Since these proteins are modulators of tumor vasculature, we explore the impact of IFN beta and p19Arf gene transfer on murine endothelial cells (tEnd). Adenovirus-mediated gene transfer of p19Arf to tEnd cells inhibited proliferation, tube formation, migration, and led to increased expression of genes related to the p53 cell death pathway, yet IFN beta gene transfer had no significant impact on tEnd viability. Alternatively, tEnd cells were exposed to the factors generated by transduced B16 (mouse melanoma) cells using either coculture or conditioned medium. In either case, transduction of B16 cells with the IFN beta vector, whether alone or in combination with p19Arf, resulted in endothelial cell death. Strikingly, treatment of tEnd cells with recombinant IFN beta did not induce death, demonstrating that additional factors produced by B16 cells contributed to the demise of tEnd cells. In this work, we have shown that our melanoma gene therapy strategy produces desirable negative effects on endothelial cells, possibly correlating with antiangiogenic activity.eng
dc.description.sponsorshipSao Paulo Research Foundation [13/25167-5, 15/26580-9, 11/21256-8, 08/55963-0, 11/10656-5]
dc.description.sponsorshipCoordenacao de Aperfeicoamento de Pessoal de Nivel Superior-Brasil (CAPES) [001]
dc.language.isoeng
dc.publisherMARY ANN LIEBERT, INCeng
dc.relation.ispartofJournal of Interferon and Cytokine Research
dc.rightsrestrictedAccesseng
dc.subjectangiogenesiseng
dc.subjectendothelial cellseng
dc.subjectmelanomaeng
dc.subjectinterferon betaeng
dc.subjectp19Arfeng
dc.subject.otheradenoviral vectoreng
dc.subject.otherstimulated geneseng
dc.subject.otherrgd-peptideeng
dc.subject.othermouse modeleng
dc.subject.otherp53eng
dc.subject.otherarfeng
dc.subject.othersuppressioneng
dc.subject.otherapoptosiseng
dc.subject.otherdeliveryeng
dc.subject.otherangiogenesiseng
dc.titleDistinct Roles of Direct Transduction Versus Exposure to the Tumor Secretome on Murine Endothelial Cells After Melanoma Gene Therapy with Interferon-beta and p19Arfeng
dc.typearticleeng
dc.rights.holderCopyright MARY ANN LIEBERT, INCeng
dc.identifier.doi10.1089/jir.2018.0124
dc.identifier.pmid30848981
dc.subject.wosBiochemistry & Molecular Biologyeng
dc.subject.wosCell Biologyeng
dc.subject.wosImmunologyeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
hcfmusp.author.externalHUNGER, Aline:Univ Sao Paulo, Fac Med, Inst Canc Estado Sao Paulo, Viral Vector Lab,Ctr Invest Translac Oncol LIM24, Sao Paulo, SP, Brazil; Cristalia, Biotecnol Unidade 1, Itapira, SP, Brazil
hcfmusp.description.beginpage246
hcfmusp.description.endpage258
hcfmusp.description.issue4
hcfmusp.description.volume39
hcfmusp.origemWOS
hcfmusp.origem.idWOS:000463643000006
hcfmusp.origem.id2-s2.0-85064072420
hcfmusp.publisher.cityNEW ROCHELLEeng
hcfmusp.publisher.countryUSAeng
hcfmusp.relation.referenceAlonso-Padilla J, 2016, MOL THER, V24, P6, DOI 10.1038/mt.2015.194eng
hcfmusp.relation.referenceBajgelman MC, 2008, VIROLOGY, V371, P8, DOI 10.1016/j.virol.2007.11.015eng
hcfmusp.relation.referenceBajgelman MC, 2013, VIROLOGY, V447, P166, DOI 10.1016/j.virol.2013.09.004eng
hcfmusp.relation.referenceBeatty MS, 2012, ADV CANCER RES, V115, P39, DOI [10.1016/B978-0-12-3983,12-8.00002-1, 10.1016/B978-0-12-398342-8.00002-1]eng
hcfmusp.relation.referenceBenedict WF, 2004, MOL THER, V10, P525, DOI 10.1016/j.ymthe.2004.05.027eng
hcfmusp.relation.referenceBracarda S, 2010, EUR J CANCER, V46, P284, DOI 10.1016/j.ejca.2009.10.013eng
hcfmusp.relation.referenceChawla-Sarkar M, 2003, APOPTOSIS, V8, P237, DOI 10.1023/A:1023668705040eng
hcfmusp.relation.referenceChipuk JE, 2005, SCIENCE, V309, P1732, DOI 10.1126/science.1114297eng
hcfmusp.relation.referenceCrystal RG, 2014, HUM GENE THER, V25, P3, DOI 10.1089/hum.2013.2527eng
hcfmusp.relation.referenceDanhier F, 2012, METHOD ENZYMOL, V508, P157, DOI 10.1016/B978-0-12-391860-4.00008-2eng
hcfmusp.relation.referenceDebidda M, 2006, J BIOL CHEM, V281, P38519, DOI 10.1074/jbc.M604607200eng
hcfmusp.relation.referenceDettin M, 2015, J PEPT SCI, V21, P786, DOI 10.1002/psc.2808eng
hcfmusp.relation.referenceDickson PV, 2007, MOL CANCER RES, V5, P531, DOI 10.1158/1541-7786.MCR-06-0259eng
hcfmusp.relation.referenceDudley AC, 2012, CSH PERSPECT MED, V2, DOI 10.1101/cshperspect.a006536eng
hcfmusp.relation.referenceELDEIRY WS, 1993, CELL, V75, P817, DOI 10.1016/0092-8674(93)90500-Peng
hcfmusp.relation.referenceGandini S, 2005, EUR J CANCER, V41, P45, DOI 10.1016/j.ejca.2004.10.016eng
hcfmusp.relation.referenceGiglia-Mari G, 2003, HUM MUTAT, V21, P217, DOI 10.1002/humu.10179eng
hcfmusp.relation.referenceGomez D, 2003, J IMMUNOL, V170, P5373, DOI 10.4049/jimmunol.170.11.5373eng
hcfmusp.relation.referenceGuo FK, 2003, J BIOL CHEM, V278, P14414, DOI 10.1074/jbc.M300341200eng
hcfmusp.relation.referenceHiggins HW, 2015, J AM ACAD DERMATOL, V73, P181, DOI 10.1016/j.jaad.2015.04.014eng
hcfmusp.relation.referenceHunger A, 2017, CELL DEATH DISCOV, V3, DOI 10.1038/cddiscovery.2017.17eng
hcfmusp.relation.referenceIzawa JI, 2002, CLIN CANCER RES, V8, P1258eng
hcfmusp.relation.referenceKamijo T, 1998, P NATL ACAD SCI USA, V95, P8292, DOI 10.1073/pnas.95.14.8292eng
hcfmusp.relation.referenceKasala D, 2014, EXPERT OPIN DRUG DEL, V11, P379, DOI 10.1517/17425247.2014.874414eng
hcfmusp.relation.referenceKawagishi H, 2010, CANCER RES, V70, P4749, DOI 10.1158/0008-5472.CAN-10-0368eng
hcfmusp.relation.referenceKhare R, 2011, CURR GENE THER, V11, P241, DOI 10.2174/156652311796150363eng
hcfmusp.relation.referenceLi JH, 2008, J MATER SCI-MATER M, V19, P2595, DOI 10.1007/s10856-007-3354-5eng
hcfmusp.relation.referenceMedrano RFV, 2017, ONCOTARGET, V8, P71249, DOI 10.18632/oncotarget.19531eng
hcfmusp.relation.referenceMerkel CA, 2013, CANCER GENE THER, V20, P317, DOI 10.1038/cgt.2013.23eng
hcfmusp.relation.referenceMichiels C, 2003, J CELL PHYSIOL, V196, P430, DOI 10.1002/jcp.10333eng
hcfmusp.relation.referenceMilojkovic A, 2013, INT J CANCER, V133, P2551, DOI 10.1002/ijc.28279eng
hcfmusp.relation.referenceMizuguchi H, 2001, GENE THER, V8, P730, DOI 10.1038/sj.gt.3301453eng
hcfmusp.relation.referenceNakano K, 2001, MOL CELL, V7, P683, DOI 10.1016/S1097-2765(01)00214-3eng
hcfmusp.relation.referencePeng HH, 2006, ANAL BIOCHEM, V354, P140, DOI 10.1016/j.ab.2006.04.032eng
hcfmusp.relation.referencePesonen S, 2012, INT J CANCER, V130, P1937, DOI 10.1002/ijc.26216eng
hcfmusp.relation.referenceCatani JPP, 2016, TRANSL ONCOL, V9, P565, DOI 10.1016/j.tranon.2016.09.011eng
hcfmusp.relation.referenceRossi UA, 2015, BIOMED PHARMACOTHER, V72, P44, DOI 10.1016/j.biopha.2015.04.002eng
hcfmusp.relation.referenceSandoval R, 2004, J BIOL CHEM, V279, P32275, DOI 10.1074/jbc.M313830200eng
hcfmusp.relation.referenceSchmid M, 2018, NAT COMMUN, V9, DOI 10.1038/s41467-017-02707-6eng
hcfmusp.relation.referenceSchmid MC, 2007, CANCER LETT, V250, P1, DOI 10.1016/j.canlet.2006.09.002eng
hcfmusp.relation.referenceSchoggins JW, 2011, CURR OPIN VIROL, V1, P519, DOI 10.1016/j.coviro.2011.10.008eng
hcfmusp.relation.referenceSiegel R, 2014, CA-CANCER J CLIN, V64, P9, DOI 10.3322/caac.21208eng
hcfmusp.relation.referenceStrauss BE, 2004, VIROLOGY, V321, P165, DOI 10.1016/j.virol.2003.12.021eng
hcfmusp.relation.referenceTakaoka A, 2003, NATURE, V424, P516, DOI 10.1038/nature01850eng
hcfmusp.relation.referenceTeodoro JG, 2007, J MOL MED-JMM, V85, P1175, DOI 10.1007/s00109-007-0221-2eng
hcfmusp.relation.referenceUlanet DB, 2010, PLOS ONE, V5, DOI 10.1371/journal.pone.0012454eng
hcfmusp.relation.referenceMedrano RFV, 2016, CANCER IMMUNOL IMMUN, V65, P371, DOI 10.1007/s00262-016-1807-8eng
hcfmusp.relation.referenceVillanueva J, 2008, CURR ONCOL REP, V10, P439, DOI 10.1007/s11912-008-0067-yeng
hcfmusp.relation.referenceZhang YP, 1998, CELL, V92, P725, DOI 10.1016/S0092-8674(00)81401-4eng
dc.description.indexMEDLINEeng
dc.identifier.eissn1557-7465
hcfmusp.citation.scopus1-
hcfmusp.scopus.lastupdate2022-06-10-
Appears in Collections:

Artigos e Materiais de Revistas Científicas - HC/ICESP
Instituto do Câncer do Estado de São Paulo - HC/ICESP

Artigos e Materiais de Revistas Científicas - LIM/24
LIM/24 - Laboratório de Oncologia Experimental

Artigos e Materiais de Revistas Científicas - ODS/03
ODS/03 - Saúde e bem-estar


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