Galectin-1 is a member of β-galactose binding lectin family and it is a dimmer with each subunit containing a carbohydrate-recognition domain. Previous studies have reported that galectin-1 expression was correlated with the aggressiveness of many kinds of cancer. However, the function of galectin-1 in tumor metastasis was not fully understood. In this study, we found that galectin-1 was highly expressed at the invasive fronts of the primary tumor and metastatic cancer cells in the lymph nodes of oral squamous cell carcinoma (OSCC) patients.Highly invasive lung adenocarinoma and OSCC cell lines exhibited more galectin-1 expression compared with less-invasive ones. The effect of galectin-1 in tumor invasion was illustrated by in vitro invasion chamber assay, where galectin-1 siRNA could reduce the invasion ability of highly invasive cancer cells and exogenous addition of galectin-1 to the less-invasive cancer cells significantly increased their invasion capacity. The mechanism study showed that stimulation of OC-2 cells (a less invasive OSCC cell line) with galectin-1 led to a dose-dependent increase in expression and secretion of matrix metalloproteinase-9 (MMP-9). The galectin-1-induced MMP-9 overexpression was through activation of MAP kinase, Erk1/2. In addition, Transforming Growth Factor-β1 (TGFβ1)-induced E-cadherin down-regulation and epithelial-mesenchymal transition (EMT) could be enhanced by co-treatment with galectin-1. Knockdown of galectin-1 in human alveolar epithelial cells (A549) increased E-cadherin expression to perturb EMT. Taken together, these results indicate that galectin-1 might promote OSCC and lung adenocarcinoma cells invasion and metastasis by up-regulating the expression of MMP-9 and favoring EMT.

98th AACR Annual Meeting-- Apr 14-18, 2007; Los Angeles, CA