Extracellular galectin-3 facilitates colon cancer cell migration and is related to the epidermal growth factor receptor.

We previously found that galectin-3 enhanced DLD-1 cell migration through the K-Ras-Raf-Erk1/2 pathway, but the effect of extracellular galectin-3 on cancer cell migration and its interaction with the epidermal growth factor receptor (EGFR) remained unknown. We aimed to determine the effect of extracellular galectin-3 on colon cancer cell migration and its correlation with the EGFR expression. Western blotting was performed to analyze galectin-3 secretion, shRNA was used to stably knock down galectin-3 expression and a migration assay was performed to evaluate colon cancer cell migration. Tissues from eighty patients with four different stages of colon cancer were obtained and compared to normal colon tissue. The galectin-3 knockdown colon cancer cells exhibited decreased migration, which was restored by recombinant galectin-3. An EGFR blocking antibody decreased colon cancer cell migration. The addition of recombinant galectin-3 increased phosphorylated EGFR expression within minutes and enhanced the internalization of the EGFR from the cell membrane to the cytoplasm, particularly upon EGF stimulation. Extracellular galectin-3 increased colon cancer cell migration, which correlated with the EGFR. Targeting galectin-3 may have a synergistic effect on EGFR-targeted therapy.