C-myc expression in dysplasias and carcinomas developed in the tongue from galectin-3-deficient and wild-type mice challenged by 4NQO

Abstract

Introduction: Oral squamous cell carcinoma is a common world-wide malignancy and its pathogenesis may be related to Wnt-protein expression and galectin-3. Likewise, the oncogenic role of galectin-3 (GAL3) can be attributed to its involvement in the Wnt signaling, especially by enhancing c-myc expression. However, no study has hitherto shown whether GAL3 interferes in the expression of this protein during oral carcinogenesis. This study reports c-myc expression in dysplasias and carcinomas developed induced in the tongue of galectin-3 deficient (GAL3)/)) and wild-type (GAL3+/+) mice. Material and Methods: Of 60 GAL3)/) and GAL3 +/+ mice were treated with 4NQO for 16 weeks and killed at week 16 and week 32. Tongues were removed and embedded in paraffin. Sections were stained with hematoxylin-eosin to diagnose dysplasias and carcinomas. An immunohistochemical assay was applied to detectc-myc in these lesions. Results: Oral carcinogenesis occurred in both groups (P > 0.05). C-myc expression was mainly observed in the cytoplasm of dysplastic and tumor cells. The intensity varied from weak, moderate to intense in both dysplasias and carcinomas. The mean of c-myc positive cells in dysplasias and carcinomas from GAL3 +/+ mice was 1.43 ± 2.05 and 1.2 ± 1.62 respectively. In GAL3)/) mice, the mean was 3.49 ± 3.20 in dysplastic lesions and 2.95 ± 2.30 in carcinomas. All differences showed to be statistically significant (P < 0.05). Conclusion: Our results revealed that the absence of GAL3 altered the c-myc expression in dysplasias and carcinomas in GAL3)/) mice when compared no alteration of c-myc expression in those lesions in GAL3 +/+ mice (FAPEMIG).