IQUIFIB   02644
INSTITUTO DE QUIMICA Y FISICOQUIMICA BIOLOGICAS "PROF. ALEJANDRO C. PALADINI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Galectin-1: Its novel contribution to hepatocellular carcinoma dissemination
Autor/es:
TRONCOSO MF
Lugar:
Villa General Belgrano, Córdoba
Reunión:
Simposio; 2nd Argentinean Glycobiology Symposium ?GlycoAr 2016?, From sugars to functions.; 2016
Resumen:
Hepatocellular carcinoma (HCC) is the third cause of cancer-related deaths annually. Although HCC treatment has improved during the past decade, its incidence still matches mortality. As metastasis is the most common cause of death among patients with this disease, it is important to explore the mechanisms underlying the spread of HCC cells for the development of new therapeutic agents. Galectin-1 (Gal-1) belongs to a family of lactose-binding lectins characterized by their affinity for β-galactoside moieties. Gal-1 is a multifunctional protein involved in different aspects of tumorigenesis. In human HCC tissues Gal-1 is up-regulated, and this overexpression correlates with HCC cell migration, tumor invasiveness, metastasis, and shortened patient survival. However, the role of Gal-1 in the molecular mechanisms leading to HCC dissemination remained uncertain. Further results obtained in our laboratory provided evidences of the involvement of Gal-1 in HCC cell adhesion, polarization, and epithelial-mesenchymal transition. Moreover, our findings revealed that Gal-1 overexpression, partly induced by transforming growth factor β1 (TGF-β1), promotes HCC cell proliferation, resistance to TGF-β1-induced growth inhibition and glycan-dependent adhesion to liver sinusoidal endothelial cells. Therefore, the novel contribution of Gal-1 to tumor hepatocyte dissemination highlights this glycan-binding protein as an interesting therapeutic target to restrain HCC progression.