Effect of galectin-3 on vasculogenic mimicry in esophageal cancer cells

Galectin-3 is a multifunctional β-galactoside binding lectin associated with tumor progression. Previous studies confirmed the roles of galecin-3 overexpression and silencing in the biological behavior of Eca109 human esophageal cancer (EC) cells; galectin-3 may serve a critical role in the vasculogenic mimicry (VM) of tumors. Therefore, the present study examined the effects of galectin-3 knockdown using lentivirus vectors on VM in EC. Eca109 and EC9706 EC cells were transfected with a lentiviral vector to inhibit galectin-3 expression, or a control vector. VM formation in vitro was evaluated via 3D culture. Western blotting was used to detect the expression level of galectin-3 following galectin-3 silencing and the expression levels of VE-cadherin, ephrin type-A receptor 2 precursor (EphA2) and matrix metalloproteinase 2 (MMP-2). According to the results of western blot analysis, the Eca109/galectin-3 and EC9706/galectin-3 cells exhibited effective galectin-3 silencing (P<0.05). Eca109 and EC9706 cells formed typical tubular networks; the number of tubular networks markedly decreased subsequent to galectin-3 knockdown. The expression levels of MMP-2 and EphA2 proteins in Eca109/galectin-3 and EC9706/galectin-3 cells were lower compared with those in Eca109, EC9706, and control vector-transfected Eca109 and EC9706 cells (P<0.05); however, there was no significant difference in the expression of VE-cadherin proteins. These results indicated that galectin-3 may modulate VM in EC by regulating the EphA2 expression level, which affects VM formation via MMP-2.