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Glycobiology Advance Access originally published online on June 12, 2006
Glycobiology 2006 16(9):810-821; doi:10.1093/glycob/cwl013
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Galectin-1: biphasic growth regulation of Leydig tumor cells

Verónica A. Biron2, M. Mercedes Iglesias2, María F. Troncoso2, Marcos Besio-Moreno3, Zoraida J. Patrignani3, Omar P. Pignataro3,4 and Carlota Wolfenstein-Todel1,2

2 Instituto de Química y Fisicoquímica Biológicas (UBA-CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956, (1113) Buenos Aires, Argentina 3 Laboratorio de Endocrinología Molecular y Transducción de Señales, Instituto de Biología y Medicina Experimental, Vuelta de Obligado 2490, (1428) Buenos Aires, Argentina; and 4 Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Pabellón II, Ciudad Universitaria, (1428) Buenos Aires, Argentina

1 To whom correspondence should be addressed; e-mail: cwtodel{at}mail.retina.ar

Received on January 27, 2006; revised on May 29, 2006; accepted on June 7, 2006

Galectin-1 (Gal-1) is a widely expressed ß-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 ({Delta}{Psi}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.

Key words: apoptosis / galectin-1 / Leydig cells / proliferation


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