De novo galectin-3 expression influences the response of melanoma cells to isatin-Schiff base copper (II) complex-induced oxidative stimulus

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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.authorBORGES, Beatriz E.
dc.contributor.authorTEIXEIRA, Veronica R.
dc.contributor.authorAPPEL, Marcia H.
dc.contributor.authorSTECLAN, Chelin A.
dc.contributor.authorRIGO, Fernanda
dc.contributor.authorNETO, Francisco Filipak
dc.contributor.authorFERREIRA, Ana M. da Costa
dc.contributor.authorCHAMMAS, Roger
dc.contributor.authorZANATA, Silvio M.
dc.contributor.authorNAKAO, Lia S.
dc.date.accessioned2014-01-28T22:20:08Z
dc.date.available2014-01-28T22:20:08Z
dc.date.issued2013
dc.description.abstractGalectin-3, a ubiquitous member of the galectin family, has been shown to control cellular proliferation, adhesion, migration and apoptosis; thus, it has.a role in tumor development and progression. Galectin-3 expression is both up- and down-regulated during melanoma progression. However, conflicting data regarding its roles in tumor biology prompted us to investigate if the presence of galectin-3 influences the response of melanoma cells to a novel metallodrug because metastatic melanoma acquires chemo resistance and is reported to be redox-sensitive. Previously, it was demonstrated that the complex [bis-(2-oxindo1-3-yl-imino)-2-(2-aminoethyl) pyridine-N,N'] copper (II) perchlorate, herein referred to as [Cu(isaepy)], induces ROS formation and apoptosis in neuroblastoma cells through mitochondrial uncoupling and the activation of AMPK/p38/p53 signaling. Here, we used a model of vertical growth melanoma (TM1), in which GAL3 expression is lost during tumor progression. When de novo expressed, galectin-3 was found to be ubiquitously present in all subcellular compartments. Our results demonstrate that de novo galectin-3 expression impairs the cellular antioxidant system and renders TM1G3 cells more susceptible than GAL3-null TM1MNG3 cells to [Cu(isaepy)] treatment. This compound, in contrast with the redox inactive [dichloro (2-oxindo1-3-yl-imino)-2-(2-aminoethyl) pyridine-N,N1 zinc (II), herein referred to as [Zn(isaepy)], leads to increased intracellular ROS accumulation, increased carbonyl stress, increased mitochondrial depolarization, decreased cell adhesion, increased p38 activation and apoptosis in TM1G3, compared with TM1MNG3. Cell death was shown to be dependent on a hydrogen peroxide-derived species and on the activation of p38. Because mitochondria are a target of both [Cu(isaepy)] and galectin-3, we propose that the presence of galectin-3 in this organelle favors increased ROS production, thereby inducing oxidative cellular damage and apoptotic death. Therefore, [Cu(isaepy)] may be envisaged as a possible anti-melanoma strategy, particularly for melanomas that express galectin-3.
dc.description.indexMEDLINE
dc.description.sponsorshipINCT Redoxoma, Fundacao Araucaria and CNPq
dc.description.sponsorshipCNPq
dc.identifier.citationCHEMICO-BIOLOGICAL INTERACTIONS, v.206, n.1, p.37-46, 2013
dc.identifier.doi10.1016/j.cbi.2013.08.005
dc.identifier.issn0009-2797
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/4028
dc.language.isoeng
dc.publisherELSEVIER IRELAND LTD
dc.relation.ispartofChemico-Biological Interactions
dc.rightsrestrictedAccess
dc.rights.holderCopyright ELSEVIER IRELAND LTD
dc.subjectGalectin-3
dc.subjectMelanoma cells
dc.subjectCopper
dc.subjectMetal complex
dc.subject.otherdecreased expression
dc.subject.othertumor progression
dc.subject.othermetastatic melanoma
dc.subject.otherprostate-cancer
dc.subject.otherbinding lectin
dc.subject.otherapoptosis
dc.subject.othercarcinoma
dc.subject.otherprotein
dc.subject.otherdamage
dc.subject.otherstress
dc.subject.wosBiochemistry & Molecular Biology
dc.subject.wosPharmacology & Pharmacy
dc.subject.wosToxicology
dc.titleDe novo galectin-3 expression influences the response of melanoma cells to isatin-Schiff base copper (II) complex-induced oxidative stimulus
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalBORGES, Beatriz E.:Univ Fed Parana, Dept Patol Basica, BR-81531980 Curitiba, Parana, Brazil
hcfmusp.author.externalTEIXEIRA, Veronica R.:Univ Sao Paulo, Fac Med, Sao Paulo, Brazil
hcfmusp.author.externalAPPEL, Marcia H.:Univ Fed Parana, Dept Patol Basica, BR-81531980 Curitiba, Parana, Brazil
hcfmusp.author.externalSTECLAN, Chelin A.:Univ Fed Parana, Dept Patol Basica, BR-81531980 Curitiba, Parana, Brazil
hcfmusp.author.externalRIGO, Fernanda:Univ Fed Parana, Dept Patol Basica, BR-81531980 Curitiba, Parana, Brazil
hcfmusp.author.externalNETO, Francisco Filipak:Univ Fed Parana, Dept Biol Celular, BR-81531980 Curitiba, Parana, Brazil
hcfmusp.author.externalFERREIRA, Ana M. da Costa:Univ Sao Paulo, Inst Quim, Sao Paulo, Brazil
hcfmusp.author.externalZANATA, Silvio M.:Univ Fed Parana, Dept Patol Basica, BR-81531980 Curitiba, Parana, Brazil
hcfmusp.author.externalNAKAO, Lia S.:Univ Fed Parana, Dept Patol Basica, BR-81531980 Curitiba, Parana, Brazil
hcfmusp.citation.scopus16
hcfmusp.contributor.author-fmusphcROGER CHAMMAS
hcfmusp.description.beginpage37
hcfmusp.description.endpage46
hcfmusp.description.issue1
hcfmusp.description.volume206
hcfmusp.origemWOS
hcfmusp.origem.pubmed23994248
hcfmusp.origem.scopus2-s2.0-84883691163
hcfmusp.origem.wosWOS:000326560700005
hcfmusp.publisher.cityCLARE
hcfmusp.publisher.countryIRELAND
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hcfmusp.remissive.sponsorshipCNPq
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