GALECTIN 1 PROMOTES TUMOR CELL MIGRATION BY ENHANCING NA+/H+ EXCHANGER ISOFORM 1 (NHE1) ACTIVITY

CROCI DO; VALLÉS PG; COSTANTINO V.V.; BOCANEGRA MV; RABINOVICH GA; GIL LORENZO AF

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

Tumor cells evade immune responses and shape local and systemic microenvironments establishing a distinctive cellular phenotype. Galectin 1 (Gal1),a glycan-binding protein, controls tumor progression by modulating tumor immunity, angiogenesis and migration through binding to specific glycan structures of cell surface receptors. In solid tumors,the Na+/H+ exchanger isoform 1 (NHE1) favors cancer progression through pH modulation.We aimed toelucidate the role of Gal1 on NHE1 regulation in murine melanoma cells and its possible role in tumor cell migration. To determine NHE1 activity we used a BCECF-AM flow cytometry kinetics assay. We observed increased NHE1 activity in melanoma cells in comparison to a non-tumorigenic cell line.To evaluate whether Gal1 could be involved in NHE1 hyperactivity, cells were treated with NHE1 inhibitor (Eipa), recombinant Gal1 (rGal1) or were silenced for Gal1 (shGal1).We observed diminished NHE1 activity after Eipa treatment with similar results obtained after shGal1 silencing (p