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E‐cadherin and β‐catenin are down‐regulated in prostatic bone metastases
Author(s) -
Bryden A.A.G.,
Hoyland J.A.,
Freemont A.J.,
Clarke N.W.,
Schembri Wismayer D.,
George N.J.R.
Publication year - 2002
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1046/j.1464-4096.2001.01712.x
Subject(s) - cadherin , catenin , prostate cancer , beta catenin , metastasis , pathology , prostate , bone metastasis , in situ hybridization , phenotype , medicine , cancer research , messenger rna , biology , cancer , wnt signaling pathway , gene , cell , biochemistry , genetics
Objective To determine the E‐cadherin and β‐catenin expression phenotype in untreated primary prostate cancer and corresponding bone metastases. Materials and methods Paired bone metastasis and primary prostate specimens were obtained from 14 men with untreated metastatic prostate carcinoma. The tumours were histologically graded by an independent pathologist. Expression of mRNA for E‐cadherin and β‐catenin was detected within the tumour cells using in‐situ hybridization with a 35 S‐labelled cDNA probe. The expression of E‐cadherin and β‐catenin were graded as uniform, heterogeneous or negative. Results The mRNA for E‐cadherin was expressed in 13 of 14 primary carcinomas and 11 bone metastases; β‐catenin was expressed by 13 and nine, respectively. Of the primary tumours, nine expressed E‐cadherin and β‐catenin uniformly; in contrast, all metastases had down‐regulated E‐cadherin and/or β‐catenin. Conclusions The down‐regulation of E‐cadherin and β‐catenin are a feature of the metastatic phenotype, which may be a significant factor in the genesis of bone metastases. However, this does not appear to be reflected in the expression of these molecules in the primary tumours.