Journal of Mammary Gland Biology and Neoplasia

, Volume 12, Issue 2, pp 127–133

Differential Cadherin Expression: Potential Markers for Epithelial to Mesenchymal Transformation During Tumor Progression

Authors

  • Georgia Agiostratidou
    • Department of PathologyAlbert Einstein College of Medicine
  • James Hulit
    • Department of PathologyAlbert Einstein College of Medicine
  • Greg R. Phillips
    • Fishberg Department of NeuroscienceMount Sinai School of Medicine
    • Department of PathologyAlbert Einstein College of Medicine
    • Albert Einstein College of Medicine
Article

DOI: 10.1007/s10911-007-9044-6

Cite this article as:
Agiostratidou, G., Hulit, J., Phillips, G.R. et al. J Mammary Gland Biol Neoplasia (2007) 12: 127. doi:10.1007/s10911-007-9044-6

Abstract

The cadherin family of adhesion molecules regulates cell–cell interactions during development and in tissues. The prototypical cadherin, E-cadherin, is responsible for maintaining interactions of epithelial cells and is frequently downregulated during tumor progression. N-cadherin, normally found in fibroblasts and neural cells, can be upregulated during tumor progression and can increase the invasiveness of tumor cells. The proinvasive effects of N-cadherin expression in tumor cells result from two possible mechanisms: promotion of tumor cell interactions with the N-cadherin-expressing microenvironment, or enhancement of signaling via the fibroblast growth factor receptor. The downregulation of E-cadherin and the upregulation of N-cadherin in tumors may be a result of an epithelial to mesenchymal transformation (EMT) of tumor cells, which is notoriously difficult to detect in vivo. Double labeling of individual tumors with specific E- and N-cadherin antibodies suggests that EMT can occur heterogeneously and/or transiently within an invasive tumor.

Keywords

AdhesionMetastasisBreast cancerSignalingInvasion

Abbreviations

EMT

epithelial to mesenchymal transition

MMP

matrix metalloprotease

EGF

epidermal growth factor

IGF

insulin growth factor

FGF

fibroblast growth factor

HGF

hepatocyte growth factor

TGFβ

transforming growth factor beta

Copyright information

© Springer Science+Business Media, LLC 2007