PT  - JOURNAL ARTICLE
AU  - JULIANA MOREIRA DE ALMEIDA SANT'ANA
AU  - ROGER CHAMMAS
AU  - FU-TONG LIU
AU  - SUELY NONOGAKI
AU  - SÉRGIO VITORINO CARDOSO
AU  - ADRIANO MOTA LOYOLA
AU  - PAULO ROGÉRIO DE FARIA
TI  - Activation of the Wnt/Beta-catenin Signaling Pathway during Oral Carcinogenesis Process Is Not Influenced by the Absence of Galectin-3 in Mice
DP  - 2011 Sep 01
TA  - Anticancer Research
PG  - 2805--2811
VI  - 31
IP  - 9
4099  - http://ar.iiarjournals.org/content/31/9/2805.short
4100  - http://ar.iiarjournals.org/content/31/9/2805.full
SO  - Anticancer Res2011 Sep 01; 31
AB  - 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.