GALECTIN-1 AND CD13 PROMOTE LIVER TUMOR-DERIVED SINUSOIDAL ENDOTHELIAL CELL MIGRATION AND TUBE FORMATION

LUCIANA SARRIAS; MIRIAM BENSO; LORENA ROCÍO GARCÍA; MARÍA VICTORIA ESPELT; GABRIEL ADRIÁN RABINOVICH; MARÍA TERESA ELOLA; MARÍA FERNANDA TRONCOSO

Buenos Aires

Congreso; Congreso Anual de Fisiología 2023; 2023

Sociedad Argentina de Fisiología

Introduction: The β-galactoside–binding protein galectin-1 (GAL1) is overexpressed in liver tumor. CD13 is a glycosylated membrane exopeptidase upregulated in endothelial cells during tumor-related angiogenesis. Previously we described that GAL1 interacts with CD13 in SKHEP1 tumor-derived liver sinusoidal endothelial cells (LSECs) in a glycan-dependent manner.Objectives: To determine GAL1 and CD13 roles in SKHEP1 LSEC migration and tube formation.Methods: Wild type (WT), CRISPR/Cas9-based CD13 knockout (CD13KO) and scrambled (SCR) SKHEP1 LSECs were treated with recombinant GAL1 (rGAL1, 100 µg/ml) or vehicle (V). In some experiments, rGAL1 was preincubated with lactose, a galectin inhibitor. Cell migration was evaluated after 15h by wound-healing assay. For tube formation assay (angiogenesis assay), cells were cultured on a basement membrane matrix (Geltrex) for 8h.Results: Cell migration was increased in WT cells treated with rGAL1 (126±4%, p