Background: The E-cadherin–catenin adhesion complex is crucial for intercellular adhesiveness and maintenance of tissue architecture. Its impairment is associated with poorly differentiated phenotype and increased invasiveness of carcinomas.
Aims: To evaluate E-cadherin, β catenin, γ catenin, and ezrin expression and its relation to histopathological features of primary and metastatic Wilms’s tumours.
Methods: Immunohistochemistry was used to determine the expression and cellular distribution of E-cadherin, β catenin, γ catenin, and ezrin in primary and metastatic Wilms’s tumours. Western blotting was used to determine polypeptide size and expression of E-cadherin and β catenin in Wilms’s tumours compared with normal kidney.
Results: Moderate expression of E-cadherin was found mainly in cytoplasm and occasionally cell membranes of dysplastic tubules, whereas low expression was seen in cytoplasm of blastemal cells. Primary and metastatic tumours showed moderate to high β catenin expression in blastemal and epithelial cells, with predominantly membranous and cytoplasmic staining. Occasional nuclear staining was noted in metastatic tumours. Low to high γ catenin and ezrin expression was seen in cytoplasm of blastemal and epithelial cells of primary and metastatic tumours. Higher amounts of 92 kDa β catenin were detected in tumours than in normal kidney. Low expression of 120 kDa E-cadherin was seen in moderately differentiated tumours, whereas expression was lacking in poorly differentiated tumours.
Conclusions: Compared with primary tumours, metastatic tumours showed lower expression of E-cadherin and γ catenin, with nuclear staining for β catenin. Low E-cadherin was associated with poorly differentiated tumours. These results suggest that abnormal expression of adhesion proteins correlates with the invasive and metastatic phenotype in Wilms’s tumours.
- Wilms’s tumour
- E-cadherin (CDH1)
- β catenin (CTNNB1)
- γ catenin (CTNNG/CTNNBIP1)
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