Expression profile of components of the β-catenin destruction complex in oral dysplasia and oral cancer

xlomafota13 shared this article with you from Inoreader Expression profile of components of the β-catenin destruction complex in oral dysplasia and oral cancer Via pubmed: "med oral patol oral... Med Oral Patol Oral Cir Bucal. 2021 Sep 25:24528. doi: 10.4317/medoral.24528. Online ahead of print. 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. PMID:34564680 | DOI:10.4317/medoral.24528 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.