| dc.description | Galectin-3 (Gal-3) is a multifunctional ??-galactoside-binding lectin that once synthesized is expressed in the nucleus, cytoplasm,
cell surface, and extracellular environment. Gal-3 plays an important role in breast cancer tumors due to its ability to promote
interactions between cell-cell and cell-extracellular matrix (ECM) elements, increasing tumor survival and metastatic dissemination.
Still, the mechanism by which Gal-3 interferes with tumor cell migration and metastasis formation is complex and not
fully understood. Here, we showed that Gal-3 knockdown increased the migration ability of 4T1 murine breast cancer cells in vitro.
Using the 4T1 orthotopic breast cancer spontaneous metastasis mouse model, we demonstrated that 4T1-derived tumors were
significantly larger in the presence of Gal-3 (scramble) in comparison with Gal-3 knockdown 4T1-derived tumors. Nevertheless,
Gal-3 knockdown 4T1 cells were outnumbered in the bone marrow in comparison with scramble 4T1 cells. Finally, we reported
here a decrease in the content of cell-surface syndecan-1 and an increase in the levels of chondroitin sulfate proteoglycans such as
versican in Gal-3 knockdown 4T1 cells both in vitro and in vivo. Overall, our findings establish that Gal-3 downregulation during
breast cancer progression regulates cell-associated and tumor microenvironment glycosaminoglycans (GAGs)/proteoglycans
(PG), thus enhancing the metastatic potential of tumor cells. | |
