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.

Highlights

  • Cutaneous melanoma accounts for 4 percent of all skin cancer

  • We verified that galectin-3 was highly expressed in murine melanoma line (B16F10 cells, Figure 1(a)) and this expression was observed in the cytoplasm of melanoma cells, by immunofluorescence (Figure 1(b))

  • Melanoma cells were injected into the subcutaneous tissue of galectin-3 knock-out and wild-type mice

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Summary

Introduction

Cutaneous melanoma accounts for 4 percent of all skin cancer It is responsible for 80 percent of deaths associated to skin malignancies [1]. The malignant transformation of melanocytes consists of multiple, complex processes characterized by changes in the expression of molecules involved in the control of cell growth, proliferation, adhesion and death [2,3]. Several lines of evidence suggest that pathogenesis of melanoma is a multistep process that may include the phases of benign nevi, dysplastic nevi, radial and vertical growth-phase melanoma and metastatic melanoma [4]. Tumor invasion and the metastatic potential of various human cancers, including melanoma, were associated with the expression of galectin-3 [5,6,7,8]

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