Contribution of Galectin-1 to hepatocellular carcinoma cell drug resistance

CARABIAS P; BACIGALUPO ML , , ; RUBIN A; SAFFIOTI NA; ELOLA MT; LANARI C; ROSSI JP; WOLFENSTEIN C; ROJAS P; RABINOVICH GA; ESPELT MV; TRONCOSO MF

Congreso; LXIII Reunión Científica Anual Sociedad Argentina de Investigación Clínica- LXVI Reunión Científica Anual Sociedad Argentina de Inmunología- Reunión Científica Anual Sociedad Argentina de Fisiología; 2018

Hepatocellular carcinoma (HCC) is characterized by a high resistance to chemotherapy. P-glycoprotein (P-gp) is an ATP-dependent drug efflux pump and its overexpression in HCC is associated with a decrease in intracellular drug concentration, leading to chemotherapeutic failure. Galectin-1 (Gal1), a β-galactoside-binding protein, is overexpressed in HCC and it is related to tumor aggressiveness. Recent studies have shown that Gal1 may have a role in HCC chemoresistance. Nevertheless the mechanisms underlying this effect remain unclear. Our aim was to investigate the molecular basis of Gal1-mediated chemoresistance in HCC cells.We stably transfected human HCC HepG2 cells to overexpress (HepG2Gal1) or silence (shRNAs) Gal1 expression, with the corresponding control cells.By inoculating cells into NSG mice we observed a decrease in the volume of control-derived tumors treated with doxorubicin (DOX,4.5 mg/kg i.v., once a week for 3 weeks) compared with HepG2Gal1-derived treated tumors (0.43±0.03cm3 vs 1.39±0.38cm3, p