Fig. 2

Schematic representation of proposed LGALS3BP functions in cancer. 1. EVs-associated LGALS3BP induces IL-6 production from bone marrow mesenchymal cells contributing to the creation of pro-tumorigenic microenvironment [60, 61, 94]. 2. LGALS3BP interacts with DC-SIGN to suppress Dendritic Cells maturation [74]. 3. LGALS3BP interacts with Siglecs receptor on immune cells stimulating immune-evasion [75]. 4. LGALS3BP is involved in inhibition of monocyte-fibrocyte differentiation [16]. 5. Free and EVs-associated LGALS3BP induces VEGF production in cancer cells via PI3K/AKT signaling promoting angiogenesis [18, 97]. 6. LGALS3BP destabilizes adherens junctions of cancer cells via dissociation of the E-cadherin–p120-catenin complex [17]. 7. LGALS3BP mediates adhesion of cancer cells to several matrix extracellular proteins like fibronectin, nidogen, laminin 1-5-10 and collagen IV [71, 85]. 8. LGALS3BP has a role in the integrins-mediated adhesion of cancer cells to endothelial cells, promoting survival, proliferation, motility and migration pathways [18, 36, 100]. 9. LGALS3BP mediates homotypic aggregation cell induced by galectin-1 and galectin-3 [9, 35]. 10. LGALS3BP is involved in E-selectin mediated adhesion to endothelial cells [14, 15]. 11. LGALS3BP promotes angiogenesis through binding to endothelial integrins and FAK activation mediated by galectin-3 [18]. 12. LGALS3BP has a role in cross-talk between tumor and stroma mediated by endosialin expressed on pericytes and activated fibroblasts [63]