Expression profile of components of the beta-catenin destruction complex in oral dysplasia and oral cancer
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2021Metadata
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Goñi, Francisca J.
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Expression profile of components of the beta-catenin destruction complex in oral dysplasia and oral cancer
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Abstract
Background: Oral cancer represents the sixth most common cancer in the world and is associated with 40-50%
survival at 5 years. Within oral malignancies, oral squamous cell carcinoma (OSCC) is commonly preceded by
potentially malignant lesions, which, according to histopathological criteria, are referred to as oral dysplasia and
their diagnosis are associated with higher rates of malignant transformation towards cancer. We recently reported
that aberrant activation of the Wnt/β catenin pathway is due to overexpression of Wnt ligands in oral dysplasia.
However, the expression of other regulators of this pathway, namely components of the β-catenin destruction
complex has not been explored in oral dysplasia.
Material and Methods: Using immunohistochemical analyses, we evaluated nuclear expression of β catenin and
its association with Wnt3a and Wnt5a. Likewise, components of the β-catenin destruction complex, including
Adenomatous Polyposis Coli (APC), Axin and Glycogen Synthase Kinase 3 beta (GSK-3β) were also evaluated
in oral dysplasia and OSCC biopsies.
Results: We found that moderate and severe dysplasia samples, which harbored increased expression of nuclear
β catenin, depicted augmented cytoplasmic expression of GSK 3β, Axin and APC, in comparison with OSCC
samples. Also, GSK-3β was found nuclear in mild dysplasia and OSCC samples, when compared with other study
samples.
Conclusions: Cytoplasmic levels of components of the β-catenin destruction complex are increased in oral dysplasia and might be responsible of augmented nuclear β catenin.
Patrocinador
Vice-rectory for Research and Devel-opment (VID) at Universidad de Chile UI-024/19
Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
CONICYT FONDECYT 1180495
3200313
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Med Oral Patol Oral Cir Bucal. 2021 Nov 1;26 (6):e729-37
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