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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Cell Transformation, Neoplastic, Galectin 3, Immunohistochemistry, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mouth Neoplasms, Signal Transduction, Wnt Proteins, beta Catenin.
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Is activation of the Wnt/beta-catenin signaling pathway during oral carcinogenesis process influenced by the absence of galectin-3 in mice? Context: 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. 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. 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).
assistant
Absence of galectin-3 does not interfere in the pattern of beta-catenin expression and therefore in the mediation of the Wnt signaling pathway. Final Decision: no