THE EXPRESSION OF P120CTN PROTEIN IN BREAST-CANCER IS INDEPENDENT OF ALPHA-CATENIN AND BETA-CATENIN AND E-CADHERIN

Citation
Da. Dillon et al., THE EXPRESSION OF P120CTN PROTEIN IN BREAST-CANCER IS INDEPENDENT OF ALPHA-CATENIN AND BETA-CATENIN AND E-CADHERIN, The American journal of pathology, 152(1), 1998, pp. 75-82
Citations number
40
Categorie Soggetti
Pathology
ISSN journal
00029440
Volume
152
Issue
1
Year of publication
1998
Pages
75 - 82
Database
ISI
SICI code
0002-9440(1998)152:1<75:TEOPPI>2.0.ZU;2-T
Abstract
Several studies have reported loss or alteration of expression of E-ca dherin in breast cancer and more recently changes in levels of express ion of the catenins. We used immunofluorescence to examine E-cadherin, alpha-catenin, beta-catenin, and p120ctn (formerly p120CAS) expressio n in 91 cases of invasive ductal carcinoma. As expected, all four prot eins co-localize to the junctional regions of the cells, Although nucl ear localization has been described for beta-catenin in colonic polyps , no examples were found in these breast cancer cases, We found that, although alteration is common in the catenins and E-cadherin, complete loss, as exemplified by E-cadherin in lobular carcinoma (where E-cadh erin is frequently mutated), is rarely seen, In contrast, the catenin- related protein p120ctn shows an expression pattern that is significan tly unrelated to the other catenins Cor E-cadherin), including complet e loss of expression in approximately 10% of the cases, No statistical ly significant correlations with traditional prognostic indicators wer e observed with any of these proteins, We conclude 1) that expression of E-cadherin and alpha- and beta-catenin are generally retained at th e membrane although frequently reduced or altered, 2) that complete lo ss of p120ctn expression is seen in approximately 10% of the cases, an d 3) that there is a significant correlation in the expression of E-ca dherin and the catenins but no correlation between these molecules and p120ctn, suggesting an absence of coordinate regulation.