Fig. 6

Gal-3, Gal-4 and Gal-8 pathways to EMT in cancer. (a) Extracellular Gal-3 promotes cell migration of colon cancer cells in a carbohydrate-dependent manner through a EGFR/K-Ras-Raf-ERK pathway. (b) Gal-3 overexpression activates a PI3K/AKT/GSK-3β/β-catenin signaling pathway that induces EMT and promotes metastasis in mice, and is uncertain whether this effect includes secreted Gal-3. (c) Runx2 overexpression enhances Gal-3 expression and promotes EMT in hepatocellular carcinoma and lung cancer cells. (d) In different cancer cell lines, extracellular Gal-3 interacts with Trop2 in a carbohydrate-dependent manner to promote the nuclear translocation of β-catenin, leading to EMT. (e) In prostate cancer, extracellular Gal-4 binds to and activates different tyrosine kinase receptors that trigger ERK and AKT pathways leading to EMT. (f) Gal-8 overexpression promotes partial EMT that stimulates cell proliferation, migration, invasion and tumor formation of MDCK cells involving an Integrin/FAK/EGFR pathway and proteasome activation through un unknown mechanism