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Clinical & Experimental Metastasis

, Volume 28, Issue 8, pp 811–818 | Cite as

Two possible mechanisms of epithelial to mesenchymal transition in invasive ductal breast cancer

  • Sylvie Dubois-Marshall
  • Jeremy S. Thomas
  • Dana Faratian
  • David J. Harrison
  • Elad KatzEmail author
Research Paper

Abstract

Epithelial to mesenchymal transition (EMT) occurs in embryogenesis and normal development. It has been predominantly described in vitro and in animal studies, but EMT is also implicated in the progression of many cancers with proposed roles in invasion, metastasis and resistance to treatment. It is closely associated with loss of epithelial-specific protein expression and up-regulation of mesenchymal proteins, but several pathways are implicated in its execution. We explored what are the expression patterns of EMT proteins in human breast cancer. We interrogated two independent cohorts enriched for high-grade, invasive, ductal breast cancers. We used quantitative immunofluorescence to study the expression of key EMT proteins. Statistical associations to define protein profiles were based on Pearson’s correlations. E-cadherin down-regulation in breast cancer was associated with β-catenin down-regulation, but not with up-regulation of mesenchymal markers. While EMT-related transcription repressors were expressed in some breast cancers, their expression did not negatively correlate with E-cadherin. Instead, an additional EMT profile was identified, composing Snail and Slug. In conclusion, EMT occurs in human breast cancer in a manner distinct to that seen in vitro. Certain EMT events are uncoupled from E-cadherin down-regulation and may constitute a novel EMT profile, which warrants further exploration.

Keywords

Epithelial-mesenchymal transition E-cadherin Breast cancer Neoplasm invasion Beta-catenin 

Notes

Acknowledgments

The authors would like to thank InHwa Um, Danielle Wilson and Helen Caldwell for their technical support throughout this study. We would also like to thank Andy Sims and Richard Meehan for their advice. Clinical materials were obtained through the auspices of the Edinburgh Experimental Cancer Medicine Centre. This work was supported by Breakthrough Breast Cancer and the Scottish Funding Council.

Conflict of interest

The authors declare no conflict of interest.

Supplementary material

10585_2011_9412_MOESM1_ESM.doc (114 kb)
Supplementary material 1 (DOC 114 kb)
10585_2011_9412_MOESM2_ESM.tif (119 kb)
Supplementary material 2 (TIFF 119 kb)
10585_2011_9412_MOESM3_ESM.docx (10 kb)
Supplementary material 3 (DOCX 10 kb)

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Copyright information

© Springer Science+Business Media B.V. 2011

Authors and Affiliations

  • Sylvie Dubois-Marshall
    • 1
  • Jeremy S. Thomas
    • 1
  • Dana Faratian
    • 1
  • David J. Harrison
    • 1
  • Elad Katz
    • 1
    Email author
  1. 1.Breakthrough Breast Cancer Research Unit and Division of Pathology, Institute of Genetics and Molecular MedicineUniversity of Edinburgh, Western General HospitalEdinburghUK

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