Integrins and adhesion molecules are responsible for the maintenance of the epithelial phenotype. Cell culture studies have reported the correlation between adhesion molecule expression and prostate carcinoma, but their role in the metastatic process is not yet known. Our aim is to study the expression profiles of these molecules and evaluate their association with the metastatic behavior of prostate adenocarcinoma.
Materials and Methods:
A Tissue Microarray containing two samples from 19 primary tumors and one from their corresponding lymph node metastases was constructed and subjected to immunohistochemical analysis of the expression of integrins, E-cadherin and β and γ-catenins. Within each case, paired analyses were also performed to evaluate gains or losses in metastasis compared to its primary tumor.
The expression of αv, αvβ3, α2β1 and γ-catenin were abnormal in almost every case. Marked loss of E-cadherin and β4 integrin was found in primary and metastatic lesions. β-catenin was normal in all primary cases and in 94% of metastases. α6 was normal in all primary tumors and metastases. α3 and α3β1 were normal in 32% of primary cases and in 53% and 6% of metastases, respectively. In paired analyses, loss of E-cadherin, β4, αv, α3β1 and αvβ3 was found in 65%, 71%, 59%, 53% and 47% of patients, respectively. Catenins and α2β1 showed maintenance of expression in most of the cases.
In this preliminary study we have shown that the loss of cell adhesion molecules can be considered a characteristic of the metastatic phenotype in prostate cancer. Larger series should be evaluated in order to confirm our findings.