Decreased ezrin and paxillin expression in human urothelial bladder tumors correlate with tumor progression.

OBJECTIVES: F-actin binding proteins ezrin and paxillin are involved in cell adhesion and cell migration/invasion. The aim of the study was to investigate their role in urothelial bladder carcinogenesis. MATERIALS AND METHODS: Expression of ezrin and paxillin was studied by immunohistochemistry in 104 and 96 cases of urothelial bladder tumors, respectively. Correlations with clinicopathologic data and expression of p53, E-cadherin, and ß-catenin were examined. RESULTS: Positive ezrin and paxillin protein expression was found in 99% and 93.7% of cases, respectively. Membranous expression of ezrin was significantly lower in high grade tumors and correlated with invasion. Multivariate analysis showed that ezrin is an independent predictor of muscularis propria invasion. Paxillin expression was significantly decreased in urothelial carcinomas compared with tumors of low malignant potential and low paxillin levels also correlated with advancing tumor stage and invasion. A statistically significant correlation was found between membranous ezrin and E-cadherin as well as between ezrin and paxillin expression in urothelial tumors. CONCLUSIONS: Down-regulation of ezrin and paxillin in urothelial bladder tumors is associated with aggressive tumor features and invasiveness.

ILK expression in human basal cell carcinoma correlates with epithelial-mesenchymal transition markers and tumour invasion.

AIMS: Epithelial-mesenchymal transition (EMT) has been known to play a significant role in tumour progression. Integrin-linked kinase (ILK) has been recently added to the growing list of EMT regulators that control some aspect of carcinogenesis. The aim was to study ILK expression and its relevance to EMT markers in human basal cell carcinoma (BCC). METHODS AND RESULTS: Paraffin-embedded tissue sections from 100 human BCC cases were processed by immunohistochemistry for the expression of ILK, E-cadherin, Snail, beta-catenin and alpha-smooth muscle actin (alpha-SMA). ILK overexpression was observed in 100% of cases and strongly correlated with tumour invasion and infiltrative BCC. Loss of membranous E-cadherin was found in 71% of cases while nuclear immunoreactivity for E-cadherin was also observed in 90% of the tumours. Snail, nuclear beta-catenin and alpha-SMA expression was detected in 100%, 99% and 97% of tumours, respectively. Aberrant expression of E-cadherin, nuclear beta-catenin and alpha-SMA correlated with BCC tumour invasion. Interestingly, there was a significant correlation between ILK expression and all the EMT markers examined. CONCLUSIONS: ILK overexpression in BCC is implicated in tumour progression probably through the induction of an EMT-related molecular profile. Nuclear localization of E-cadherin in BCC is also associated with aggressive tumour features.