The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype.
BACKGROUND: Currently available methods for diagnosis and staging of prostate cancer lack the sensitivity to distinguish between patients with indolent prostate cancer and those requiring radical treatment. Alterations in key adherens (AJ) and tight junction (TJ) components have been hailed as poten...
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doaj-457a4e902c1647e49de21c4434d900fa2020-11-25T01:20:49ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-01812e8166610.1371/journal.pone.0081666The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype.Claire MorganSpencer A JenkinsHoward G KynastonShareen H DoakBACKGROUND: Currently available methods for diagnosis and staging of prostate cancer lack the sensitivity to distinguish between patients with indolent prostate cancer and those requiring radical treatment. Alterations in key adherens (AJ) and tight junction (TJ) components have been hailed as potential biomarkers for prostate cancer progression but the majority of research has been carried out on individual molecules. OBJECTIVE: To elucidate a panel of biomarkers that may help distinguish dormant prostate cancer from aggressive metastatic disease. METHODS: We analysed the expression of 7 well known AJ and TJ components in cell lines derived from normal prostate epithelial tissue (PNT2), non-invasive (CAHPV-10) and invasive prostate cancer (LNCaP, DU145, PC-3) using gene expression, western blotting and immunofluorescence techniques. RESULTS: Claudin 7, α -catenin and β-catenin protein expression were not significantly different between CAHPV-10 cells and PNT2 cells. However, in PC-3 cells, protein levels for claudin 7, α -catenin were significantly down regulated (-1.5 fold, p = <.001) or undetectable respectively. Immunofluoresence showed β-catenin localisation in PC-3 cells to be cytoplasmic as opposed to membraneous. CONCLUSION: These results suggest aberrant Claudin 7, α - and β-catenin expression and/or localisation patterns may be putative markers for distinguishing localised prostate cancer from aggressive metastatic disease when used collectively.http://europepmc.org/articles/PMC3864842?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Claire Morgan Spencer A Jenkins Howard G Kynaston Shareen H Doak |
spellingShingle |
Claire Morgan Spencer A Jenkins Howard G Kynaston Shareen H Doak The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype. PLoS ONE |
author_facet |
Claire Morgan Spencer A Jenkins Howard G Kynaston Shareen H Doak |
author_sort |
Claire Morgan |
title |
The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype. |
title_short |
The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype. |
title_full |
The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype. |
title_fullStr |
The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype. |
title_full_unstemmed |
The role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype. |
title_sort |
role of adhesion molecules as biomarkers for the aggressive prostate cancer phenotype. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2013-01-01 |
description |
BACKGROUND: Currently available methods for diagnosis and staging of prostate cancer lack the sensitivity to distinguish between patients with indolent prostate cancer and those requiring radical treatment. Alterations in key adherens (AJ) and tight junction (TJ) components have been hailed as potential biomarkers for prostate cancer progression but the majority of research has been carried out on individual molecules. OBJECTIVE: To elucidate a panel of biomarkers that may help distinguish dormant prostate cancer from aggressive metastatic disease. METHODS: We analysed the expression of 7 well known AJ and TJ components in cell lines derived from normal prostate epithelial tissue (PNT2), non-invasive (CAHPV-10) and invasive prostate cancer (LNCaP, DU145, PC-3) using gene expression, western blotting and immunofluorescence techniques. RESULTS: Claudin 7, α -catenin and β-catenin protein expression were not significantly different between CAHPV-10 cells and PNT2 cells. However, in PC-3 cells, protein levels for claudin 7, α -catenin were significantly down regulated (-1.5 fold, p = <.001) or undetectable respectively. Immunofluoresence showed β-catenin localisation in PC-3 cells to be cytoplasmic as opposed to membraneous. CONCLUSION: These results suggest aberrant Claudin 7, α - and β-catenin expression and/or localisation patterns may be putative markers for distinguishing localised prostate cancer from aggressive metastatic disease when used collectively. |
url |
http://europepmc.org/articles/PMC3864842?pdf=render |
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