Galectin-1 (Gal-1) is a widely expressed
beta-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 (DeltaPsim),
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.