earticle

영어

To metastasize, tumor cells must acquire abilities to penetrate surrounding normal tissues and overcome barriers of dissemination and distant growth such as invasion, anoikis resistance, evasion of immune surveillance, extravasation, colonization, and growth in new microenvironments. Recent evidence suggests that galectin-3, a galactose binding protein, can promote metastasis by regulating detachment of cancer cells. Moreover, highly metastatic human breast cancer cells show higher levels of expression of galectin-3 and overexpression of galectin-3 enhances cell motility and invasiveness in lung cancer cells, suggesting that galectin-3 regulates cancer metastasis. However, the mechanism by which galectin-3 promotes metastasis has not been fully understood. We demonstrated here that overexpression of galectin-3 induced Epithelial-to-Mesenchymal Transition (EMT) and EMT induced by galectin-3 overexpression was remarkable in serum deprivation condition. The cell-cell adhesion molecule E-cadherin is stabilized by linking intracellularly with the actin cytoskeleton but overexpression of galectin-3 weakened the interaction of E-cadherin with cytoskeleton. Additionally, we found that galectin-3 overexpressing HT-29 cells were more resistant to anoikis stress and serum deprivation than parental HT-29 cells. Based on these findings we propose that galectin-3 is an important molecule that regulates cancer metastasis through induction of EMT and anoikis resistance.