Evaluation of the expression of integrins and cell adhesion molecules through tissue microarray in lymph node metastases of prostate cancer

• Published in: Journal of carcinogenesis 2009, Vol.8 (1), p.3-3
• Main Authors: Pontes-Junior, Jose, Reis, Sabrina Thalita, Dall'Oglio, Marcos, Neves de Oliveira, Luis Carlos, Cury, Jose, Carvalho, Paulo Afonso, Ribeiro-Filho, Leopoldo Alves, Moreira Leite, Katia Ramos, Srougi, Miguel
• Format: Article
• Language: English
• Subjects: Original
• ISSN: 1477-3163; 0974-6773; 1477-3163
• DOI: 10.4103/1477-3163.48453

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. 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 beta and gamma-catenins. Within each case, paired analyses were also performed to evaluate gains or losses in metastasis compared to its primary tumor. The expression of av, alphavbeta 3, alpha2beta 1 and gamma-catenin were abnormal in almost every case. Marked loss of E-cadherin and beta 4 integrin was found in primary and metastatic lesions. beta -catenin was normal in all primary cases and in 94% of metastases. a6 was normal in all primary tumors and metastases. alpha3 and alpha3beta 1 were normal in 32% of primary cases and in 53% and 6% of metastases, respectively. In paired analyses, loss of E-cadherin, beta 4, alphav, alpha3beta 1 and alphavbeta 3 was found in 65%, 71%, 59%, 53% and 47% of patients, respectively. Catenins and alpha2beta 1 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.