Altered expression of the pro-inflammatory enzyme cyclooxygenase (COX)-2, E-Cadherin cell-cell adhesion protein and Human epidermal growth factor receptor 2 (HER-2/neu, a proto-oncogene) are involved in the pathogenesis of several cancers including the prostatic adenocarcinoma (PRCa). However, to date the results of the previous studies in this neoplasm are controversial, and the relationships among expression of these molecules in benign prostatic hyperplasia (BPH) and PRCa are mostly unknown. We hypothesize that "there are alterations of COX-2, HER-2/neu and E-Cadherin protein expression in PRCa". We carried out this study to test our hypothesis and to assess the relationships among these molecules both in PRCa and BPH. We used immunohistochemistry to evaluate the expression of these proteins in the tissue specimens of both BPH (27 cases) and PRCa (45 cases). Immunohistochemical staining patterns verified over-expression of COX-2 and HER-2/neu proteins in PRCa as compared to BPH. Alternatively, there was an aberrant (reduced) E-Cadherin protein expression in PRCa. There were weak positive correlations between COX-2 versus HER-2/neu expression. A weak negative correlation was noted between COX-2 and E-Cadherin expression. In conclusion, there were alterations of COX-2, HER-2/neu and E-Cadherin proteins in PRCa. The molecular alterations of the relevant genes and the therapeutic ramifications (the development of selective inhibitors to COX-2 and HER-2/neu) of these preliminary findings are open to further investigations.
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Altered expression of the pro-inflammatory enzyme cyclooxygenase (COX)-2, E-Cadherin cell-cell adhesion protein and Human epidermal growth factor receptor 2 (HER-2/neu, a proto-oncogene) are involved in the pathogenesis of several cancers including the prostatic adenocarcinoma (PRCa). However, to date the results of the previous studies in this neoplasm are controversial, and the relationships among expression of these molecules in benign prostatic hyperplasia (BPH) and PRCa are mostly unknown. We hypothesize that "there are alterations of COX-2, HER-2/neu and E-Cadherin protein expression in PRCa".
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