E-cadherin, N-cadherin and ADAM12 in localized prostate cancer: A clinicopathological study

Abstract

Prostate cancer (PC) is the most prevalent cancer and the second leading cause of death in males worldwide. One of the processes responsible for its mortality is the metastasizing capacity of malignant cells, which is associated with the epithelial-mesenchymal transition process (EMT). EMT is a physiological process during embryogenesis, with loss of cell adhesion molecules such as cadherins, and overexpression of molecules associated with invasive behaviour, such as matrix metalloproteinases (MMPs). We analyzed 321 tissue samples using immunohistochemistry. E-cadherin expression was significantly lower in PC than in BPH (107.1 ± 60.0 vs. 139.99 ± 36.65; p < 0.0001), while N-cadherin was expressed in all PC samples and only in 50 % of BPH, with significantly higher intensity in PC (65.04 ± 62.2 vs. 21.23 ± 35.8; p < 0.00001). ADAM12 expression was also significantly higher in PC (113.07 ± 63.26 vs. 37.54 ± 51.59; p < 0.00001). No significant associations were found between E-cadherin and PSA and Gleason score (p > 0.17). N-cadherin and ADAM12 showed statistically significant associations with PSA (p = 0.038 and p = 0.013, respectively) but not with other clinical variables. These findings support the involvement of EMT-related markers in PC and suggest their potential utility in biological characterization, although further studies are required to determine their prognostic value.

Keywords: ADAM12; Benign prostatic hyperplasia (BPH); E-Cadherin; Epithelial-mesenchymal transition (EMT); Gleason; N-Cadherin; Prostate cancer (PC); Prostate-specific antigen (PSA).