Breast carcinomas that co-express E- and P-cadherin are associated with p120-catenin cytoplasmic localisation and poor patient survival
- 1Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal
- 2Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal
- 3Hospital Xeral-Cíes, Vigo, Spain
- 4Medical Faculty, University of Porto, Porto, Portugal
- Dr J Paredes, Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Rua Roberto Frias S/N, 4200, Porto, Portugal;
- Accepted 17 March 2008
- Published Online First 1 April 2008
Background: Changes in junctional catenin expression may compromise cadherin-mediated adhesion, increasing cell malignant properties such as invasive and metastatic abilities. Altered expression of α-, β-, γ- and p120-catenin has been reported to be associated with E-cadherin loss or decreased expression, in both breast carcinomas and breast cancer cell lines.
Aims and Methods: To investigate the expression and subcellular localisation of p120- and β-catenin in a series of human invasive breast carcinomas, and correlate it with biological markers and clinicopathological parameters.
Results: Both catenins frequently exhibited a reduced membranous or cytoplasmic staining pattern. These alterations were significantly correlated with lack of both E-cadherin and oestrogen receptor-α expression. It was possible to associate the expression of β-catenin with histological grade, tumour size and nodal status, suggesting a relevant role for this catenin as a prognostic factor. The majority of E- and P-cadherin co-expressing tumours were related to cytoplasmic expression of p120-catenin; in this group of breast carcinomas, patient survival was poor.
Conclusion: Results indicate that p120-catenin cytoplasmic accumulation may play an important role in mediating the oncogenic effects derived from P-cadherin aberrant expression, including enhanced motility and invasion, particularly in tumours which maintain E-cadherin expression.
Competing interests: None.
Funding: This work was supported by three research grants (JP: SFRH/BPD/15319/2005; ALC: POCI/N/07.01.02/10/25/2005; ASR: POCI/BIA-BCM/59252/2004) and by a scientific project (POCI/BIA-BCM/59252/2004), all financed by the Portuguese Science and Technology Foundation. We are grateful to the Calouste Gulbenkian Foundation for the “Programa Gulbenkian de Estímulo à Investigação (FCG 55/05)”.