Galectin-3 expression favors metastasis in murine melanoma

Abstract

Galectin-3 is a member of the lectin family that binds β -galactosides and plays an important role in several types of tumors. Melanoma is an invasive cancer responsible for 80% of deaths associated to skin cancers. There are some evidences that galectin-3 interacts with β -catenin, a molecule involved with Wnt signaling pathway. Here, we evaluate the role of galectin-3 intumor growth and metastasis, as well as its interaction with β -catenin. Murine melanoma cells (B16F10) were injected subcutaneously and intravenously in male C57BL/6 wild-type (WT) and galectin-3 knock-out (KO) mice. Tumor growth and lung melanoma colonies were assessed. The expression of galectin-3 and β -catenin was evaluated by immuno-histochemistry. We observed that tumor growth did not differ between the groups. However, to metastasis, the number of lung colonies in WT mice was significantly increased in comparison to that observed in KO mice. The cytoplasm expression of galectin-3 was observed in subcutaneous and metastatic tumors, w in both groups. We observed its nuclear expression in some of subcutaneous tumors of KO mice. The expression of β -catenin was detected in cell membrane of all subcutaneous tumors analyzed, whereas in the metastatic tumors we observed both cytoplasm and cell membrane staining. Altogether, our data suggest that galectin-3 favors the metastasis of melanoma cells and this process is not associated with β -catenin.