Overexpression of E‐cadherin and β‐Catenin proteins in metastatic prostate cancer cells in bone

Abstract

BACKGROUND. The expression of E-cadherin in the intercellular adhesion of metastatic prostate cancer cells in bone, which is the most prevalent site of metastatic growth, remains elusive. METHODS. The aim of the study was to compare the concurrent membranous expression of E-cadherin and b-catenin proteins, the state which is known to be associated with the cellular adhesion function of E-cadherin, in prostate biopsy tissue specimens by immunohistochemical staining method. The expression patterns of E-cadherin or b-catenin were classified as homogeneous (most cells exhibiting positively), heterogeneous (a few scattered patches of cells with positivity) or negative. RESULTS. Benign prostate hyperplasia cells exhibited homogeneous expression of both E-cadherin and b-catenin in 9 of 11 (82%), whereas the primary prostate cancer cells were homogeneously positive for both proteins only in 4 of 22 (18%) of the cases. The results are similar to those reported in literature. However, in contrast to the primary cancer, a significantly increased frequency of the metastatic prostate cancer cells in bone exhibited homogeneous expression of E-cadherin and b-catenin in 12 of 17 (71%) of the cases. A statistically significant association was observed between the overexpression of both proteins and the metastatic prostate cancer cells in bone (Fisher's exact P < 0.001). CONCLUSIONS. The result of the study demonstrated for the first time that the membranous overexpression of E-cadherin and b-catenin are significantly associated with the metastatic prostate cancer cells in bone and that the high frequency of expression suggest their involvement in the intercellular adhesion of the metastatic cells in bone.

Cellular Plasticity in Prostate Cancer Bone Metastasis

“…Six studies [45, 46, 49–51, 53] investigated the differential expression of E-cadherin in PC bone metastases. Two of these reported lower expression of E-cadherin in bone metastasis tissues compared to matched primary PC tissues [46, 51].…”

Network-based prediction for sources of transcriptional dysregulation using latent pathway identification analysis

“…Tu et al (18) demonstrated that dysregulation of TGF-β signaling in prostate cancer plays a causal role in promoting tumor metastasis. Catenin, mediated by Wnt signaling, serves two cellular roles: the first in conjunction with T-cell factors (TCF) in the transcription control of proteins key to cell proliferation and the second as a part of a complex with E-cadherin, an extracellular binding matrix that promotes intercellular adhesion (19,20). Adherens junction is the process by which E-cadherin mediates cell adhesion in tissue required for morphological changes leading to changes in the phenotype (11,19,20).…”

“…Catenin, mediated by Wnt signaling, serves two cellular roles: the first in conjunction with T-cell factors (TCF) in the transcription control of proteins key to cell proliferation and the second as a part of a complex with E-cadherin, an extracellular binding matrix that promotes intercellular adhesion (19,20). Adherens junction is the process by which E-cadherin mediates cell adhesion in tissue required for morphological changes leading to changes in the phenotype (11,19,20). Lastly, tight junction mediates cell motility, and research [these mechanisms are reviewed in the study by Martin and Jiang (21)] shows a significant role for tight junctions in maintaining cell-to-cell integrity, such that perturbations can lead to invasion and metastasis of cancer cells.…”

Expression of E-Cadherin, Cox-2, P53 and BCL-2 in Prostate Carcinomas: Correlation with Tumor Differentiation and Metastatic Potential

“…Saha et al (27) reported that loss of e-cadherin gene expression is caused by reversible epigenetic mechanisms, and showed that e-cadherin gene expression was present in metastatic bone lesions of prostate carcinoma. it was hypothesized that e-cadherin gene expression might be the last fact to provide advantage tumor cells to make clusters in metastatic areas (26). these recent studies raise doubt on the suppressor role of e-cadherin on metastasis and invasion.…”