Galectin-9 isoforms influence the adhesion between colon carcinoma LoVo cells and human umbilical vein endothelial cells in vitro by regulating the expression of E-selectin in LoVo cells

Abstract

To study the regulatory effect of galectin-9 isoforms on some molecules involved in cell adhesion/invasion, and the influence of this regulation action on the adhesion between colon carcinoma LoVo cells and human umbilical vein endothelial cells (HUVECs) in vitro. Various expression vectors of galectin-9 isoforms were transfected into LoVo cells. 24 h after transfection, the expression of integrin-beta1, E-cadherin, E-selectin, ICAM-1, CD44 and MMP-9 was detected by RT-PCR and Western blot analysis. LoVo cell-HUVEC adhesion assay was performed under conditions of galectin-9 transfection, galectin-9 transfection + galectin-9 antibody, galectin-9 transfection + E-selectin antibody and galectin-9 transfection + beta-lactose, respectively. Galectin-9L down-regulates the mRNA and protein levels of E-selectin while galectin-9M and galectin-9S up-regulate the expression of E-selectin. In LoVo cell-HUVEC adhesion assay, the average fluorescence intensity of vector transfection group, galectin-9L transfection group, galectin-9M transfection group and galectin-9S transfection group was 0.90 +/- 0.20, 0.94 +/- 0.24, 1.60 +/- 0.11 and 1.45 +/- 0.13, respectively, indicating that galectin-9M and galectin-9S facilitated the adherence of LoVo cells to HUVECs (P < 0.05). E-selectin antibody, galectin-9 antibody or beta-lactose inhibited that effect. Galectin-9 isoforms regulate the E-selectin expression in LoVo cells differently and thus influence the adhesion between LoVo cells and HUVECs in vitro in different modes. The mechanisms through which galectin-9 isoforms participate in the metastasis process of colon cancer may not be the same.