Possible roles of endothelial galectins in 3 mainstays of tumorigenesis. Schematic overview of the mechanisms by which galectin expression by activated ECs might contribute to 3 key processes in tumor progression. (A) Galectin-1, galectin-3, and galectin-9 can modulate the antitumor immune response both positively and negatively. They mainly regulate T-cell survival, activation, and transendothelial migration. In addition, they could facilitate adhesion of neutrophils and eosinophils or act as chemoattractants for macrophages and eosinophils. The overall effect possibly allows tumor cells to escape from immune surveillance. (B) Endothelial galectins have also been suggested to facilitate metastasis formation by promoting heterotypic cell adhesion between circulating tumor cells and ECs. Furthermore, the adhesion of circulating cells to ECs could stimulate the endothelial expression of galectin-1 and galectin-3. (C) Galectin-1 and galectin-3 have been shown to be involved in tumor angiogenesis. They can influence EC migration and proliferation, thereby promoting tube formation. In addition, galectin-3 acts as a chemoattractant for ECs.