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Breast carcinomas that co-express E- and P-cadherin are associated with p120-catenin cytoplasmic localisation and poor patient survival
  1. J Paredes1,2,
  2. A L Correia1,
  3. A S Ribeiro2,
  4. F Milanezi1,2,
  5. J Cameselle-Teijeiro3,
  6. F C Schmitt1,2,4
  1. 1
    Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal
  2. 2
    Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal
  3. 3
    Hospital Xeral-Cíes, Vigo, Spain
  4. 4
    Medical Faculty, University of Porto, Porto, Portugal
  1. Dr J Paredes, Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Rua Roberto Frias S/N, 4200, Porto, Portugal; jparedes{at}ipatimup.pt

Abstract

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.

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Footnotes

  • 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)”.

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