Galectin-1: Biphasic growth regulation of Leydig tumor cells

Galectin-1 (Gal-1) is a widely expressed β-galactoside-binding protein that exerts pleiotropic biological functions. To gain insight into the potential role of Gal-1 as a novel modulator of Leydig cells, we investigated its effect on the growth and death of MA-10 tumor Leydig cells. In this study, w...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Biron, V.A., Iglesias, M., Troncoso, M.F., Besio-Moreno, M., Patrignani, Z.J., Pignataro, O.P., Wolfenstein-Todel, C.
Formato: Artículo publishedVersion
Publicado: 2006
Materias:
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_09596658_v16_n9_p810_Biron
http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=artiaex&d=paper_09596658_v16_n9_p810_Biron_oai
Aporte de:
Descripción
Sumario:Galectin-1 (Gal-1) is a widely expressed β-galactoside-binding protein that exerts pleiotropic biological functions. To gain insight into the potential role of Gal-1 as a novel modulator of Leydig cells, we investigated its effect on the growth and death of MA-10 tumor Leydig cells. In this study, we identified cytoplasmic Gal-1 expression in these tumor cells by cytofluorometry. DNA fragmentation, caspase-3, -8, and -9 activation, loss of mitochondrial membrane potential (ΔΨ m), cytochrome c (Cyt c) release, and FasL expression suggested that relatively high concentrations of exogenously added recombinant Gal-1 (rGal-1) induced apoptosis by the mitochondrial and death receptor pathways. These pathways were independently activated, as the presence of the inhibitor of caspase-8 or -9 only partially prevented Gal-1-effect. On the contrary, low concentrations of Gal-1 significantly promoted cell proliferation, without inducing cell death. Importantly, the presence of the disaccharide lactose prevented Gal-1 effects, suggesting the involvement of the carbohydrate recognition domain (CRD). This study provides strong evidence that Gal-1 is a novel biphasic regulator of Leydig tumor cell number, suggesting a novel role for Gal-1 in the reproductive physiopathology. © Copyright 2006 Oxford University Press.