Activation of the Wnt/Beta-catenin signaling pathway during oral carcinogenesis process is not influenced by the absence of galectin-3 in mice

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 Galo3^-/- 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.