Journal of Mammary Gland Biology and Neoplasia

, Volume 12, Issue 2, pp 127-133

First online:

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

  • Georgia AgiostratidouAffiliated withDepartment of Pathology, Albert Einstein College of Medicine
  • , James HulitAffiliated withDepartment of Pathology, Albert Einstein College of Medicine
  • , Greg R. PhillipsAffiliated withFishberg Department of Neuroscience, Mount Sinai School of Medicine
  • , Rachel B. HazanAffiliated withDepartment of Pathology, Albert Einstein College of MedicineAlbert Einstein College of Medicine Email author 

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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.


Adhesion Metastasis Breast cancer Signaling Invasion