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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art_CHAMMAS_De_novo_galectin_3_expression_influences_the_response_2013.PDF (1.41 MB)
Citações na Scopus
16
Tipo de produção
article
Data de publicação
2013
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER IRELAND LTD
Autores
BORGES, Beatriz E.
TEIXEIRA, Veronica R.
APPEL, Marcia H.
STECLAN, Chelin A.
RIGO, Fernanda
NETO, Francisco Filipak
FERREIRA, Ana M. da Costa
ZANATA, Silvio M.
NAKAO, Lia S.
Citação
CHEMICO-BIOLOGICAL INTERACTIONS, v.206, n.1, p.37-46, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Galectin-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.
Palavras-chave
Galectin-3, Melanoma cells, Copper, Metal complex
URI
https://observatorio.fm.usp.br/handle/OPI/4028
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Coleções
Artigos e Materiais de Revistas Científicas - FM/MDR
Artigos e Materiais de Revistas Científicas - LIM/24
Artigos e Materiais de Revistas Científicas - ODS/03