Fig. 3

Galectin pathways to tissue repair involving EMT. (a) Gal-2 and Gal-4 promote wound healing very likely involving glycan-mediated cell surface interactions and TGF-β-mediated signaling, as their effects are blocked by lactose and antibodies against TGF-β; (b) Gal-3 activates the α3β1 integrin/FAK/Rac1 pathway in a carbohydrate-dependent manner to promote re-epithelialization; (c) Gal-3 promotes the formation of β4-integrin/laminin332/EGFR clusters leading to ERK signaling activation, enhancing cell migration in a carbohydrate dependent manner. It also links EGFR to ALIX function that may be involved in EGFR pathway to endocytic recycling; (d) Extracellular Gal-3 binds to CD147 promoting detachment of retinal pigment epithelial cells from the epithelia in a carbohydrate-dependent manner through an unknown signaling pathway; (e) Matrix metalloproteinase MMP-7 can control Gal-3 function through degradation, as shown in wound closure experiments with colon cancer epithelial cells; (f) Gal-7 interacts with E-cadherin stabilizing its location on the plasma membrane and favoring collective cell migration in a carbohydrate-independent manner, as shown by the lack of lactose blocking effect