Background/aim: Galectin-3 has been associated with activated Wnt pathway, translocating beta-catenin into the nucleus. However, it is still unknown whether this lectin drives the Wnt signaling activation in lesions from galectin-3-deficient (Gal3⁻/⁻) mice. The purpose was to study beta-catenin expression in tongue lesions from Gal3⁻/⁻ and wild-type (Gal3⁺/⁺) mice and the status of Wnt signaling.
Materials and methods: Twenty Gal3⁻/⁻ and Gal3⁺/⁺ male mice were challenged with 4-nitroquinolin-1-oxide and killed at week 16 and 32. Tongues were processed and stained with H&E to detect dysplasias and carcinomas. An imunohistochemical assay was performed to evaluate beta-catenin expression.
Results: Carcinomas were more evident in Gal3⁺/⁺ than Gal3⁻/⁻ mice (55.5% vs. 28.5%, respectively; p>0.05). Elevated expression of non-membranous beta-catenin was observed in dysplasias and carcinomas from both groups (p>0.05).
Conclusion: Absence of galectin-3 does not interfere in the pattern of beta-catenin expression and therefore in the mediation of the Wnt signaling pathway.