Unraveling the role of Prohibitin-1, a novel ligand of galectin-1 in hepatocellular carcinoma cell viability

OTERO S; BACIGALUPO ML; CARABIAS P; ELOLA MT; WOLFENSTEIN DE TODEL C; PASQUINI L; ESPELT MV; TRONCOSO MF

CABA

Congreso; Reunión Conjunta de Sociedades Biomédicas; 2017

Galectin-1 (Gal1) is a glycan-binding protein overexpressed in hepatocellular carcinoma (HCC). We demonstrated that Gal1 upregulation in human HCC cells induces cell proliferation, epithelial-mesenchymal transition, tumor growth and metastasis. By proteomics we have identified prohibitin-1 (PHB) as a new Gal1 ligand in HCC cells. PHB has multiple functions depending on its subcellular localization. Its role in cancer is mixed and controversial. It was found downregulated in most human HCC tissues analyzed but in other HCC samples its overexpression was observed. Liver-specific PHB knockout (KO) mice develop HCC spontaneously suggesting that PHB functions as tumor suppressor. But when highly expressed, it promotes HCC cell migration in vitro showing its involvement in tumor progression. Thus, we aimed to elucidate PHB role in HCC cell viability and to analyze if PHB expression is regulated by Gal1. By immunofluorescence we observed that PHB localizes in a punctate pattern in human HepG2 and HuH-7 HCC cells, both nuclei and cytoplasm. By siRNA transfection we downregulated PHB expression in these cells: HepG2-siPHB 31±15 vs HepG2-siControl 76±19% (p