Absence of galectin-3 does not affect the development of experimental tongue carcinomas in mice

Abstract

BackgroundGalectin-3 is a lectin that presents pivotal roles in tumor biology and there are no studies evaluating their expression in dysplasias and carcinomas developed from tongue carcinogenesis models. AimsTo investigate the role of galectin-3 in the development of tongue carcinomas using a mouse model of oral carcinogenesis. MethodsGalectin-3-deficient (gal3−/−) and wild-type (gal3+/+) mice were challenged with 4-nitroquinoline-1-oxide in drinking water for 16weeks and killed at different times. Tongues were removed and the number of dysplasias and carcinomas was counted. An immunohistochemical study for galectin-3 was performed only in the tongue from gal3+/+ mice. ResultsIn both groups, a reduction of dysplasias and an increase of carcinomas from week 16 to week 32 (p>0.05) were observed. A predominance of high cytoplasmic and nuclear galectin-3 expression was observed in carcinomas (64.7%) and dysplasias (55.5%), respectively (p>0.05). The perilesional areas always presented a statistical cytoplasmic and nuclear galectin-3 overexpression. ConclusionsAbsence of galectin-3 did not directly affect the process of carcinogenesis and a cytoplasm shift of galectin-3 seems to be associated with development of tongue carcinomas.