Except one case of salivary gland AdCC that showed loss of β-catenin expression and developed subsequent metastasis, all AdCCs showed strong and diffuse membranous β-catenin expression.
This study analyzed possible CTNNB1 mutations in salivary gland pleomorphic adenomas (PAs) and adenoid cystic carcinomas (ACCs), and determined possible differences in β-catenin immunoexpression in relation to these mutations, as well as histopathological aspects of these tumors.
Because the regulatory subunits of protein phosphatase 2A (PP2A) drive Wnt signalling via target molecules, including β-catenin, we used qRT-PCR and immunoblot analysis to investigate the expression of these subunits in an AdCC cell line (ACCS) and a more aggressive subline (ACCS-M).
Our results suggest that disturbances in the distribution of beta-catenin and E-cadherin might affect the morphology ofACC and that a small fraction of cases of ACC are characterized by a mutation in the beta-catenin gene, which is associated with the nuclear accumulation of the product of this gene but does not affect the transcription of the gene for cyclin-D1.
In this study, we investigated possible mutations in the genes for components of this pathway, namely, CTNNB1 (the gene for beta-catenin), AXIN1, and APC, in adenoid cystic carcinoma, by PCR, analysis of single-strand conformational polymorphism, and sequencing.