Volume 4 Supplement 2

Abstracts of the 16th International Charles Heidelberger Symposium on Cancer Research

Open Access

Co-expression of E- and P-cadherin in breast cancer: role as an invasion suppressor or as an invasion promoter?

  • Ana S Ribeiro1Email author,
  • Laura C Carreto2,
  • André Albergaria1,
  • Bárbara Sousa1,
  • Sara Ricardo1,
  • Fernanda Milanezi1,
  • Raquel Seruca1,
  • Manuel A Santos2,
  • Fernando Schmitt1, 3 and
  • Joana Paredes1
BMC Proceedings20104(Suppl 2):P47

DOI: 10.1186/1753-6561-4-S2-P47

Published: 24 September 2010

Cadherins are cell-cell adhesion molecules. During tumor progression, their expression and/or function are frequently altered. E-cadherin down-regulation is often associated with tumor initiation and progression in breast cancer [1], whereas P-cadherin overexpression is associated with a worse patient survival [2] and with invasive breast cancer cells [3].

In this study, we aimed to understand if P-cadherin overexpression could interfere with E-cadherin invasion suppressor role in breast cancer.

Therefore, E- and P-cadherin expression was evaluated in a series of invasive breast carcinomas. P-cadherin overexpressing tumors often do not loose E-cadherin and tumors co-expressing both cadherins showed a more aggressive behavior and were related with the worst patient survival. Further, we performed in vitro studies by silencing both cadherins in BT-20 breast cancer cells. E- and P-cadherin co-expressing breast cancer cells showed increased cell invasion and migration capacities, when compared with the ones expressing only one cadherin. P-cadherin silencing led to increased levels of cell death, demonstrating it as a cancer cell survival signal. Also, microarrays of BT-20 cells, after E- and/or P-cadherin silencing, showed that the role of each cadherin alone is distinct from when these are co-expressed in the same cell, conferring different transcriptional programs.

We can conclude that E- and P-cadherin co-expression has an invasion promoter role in breast cancer cells and is a poor patient prognostic biomarker.

Authors’ Affiliations

IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto
Department of Biology and CESAM, University of Aveiro
Medical Faculty of the University of Porto


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© Ribeiro et al; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd.