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J Clin Med. 2015 Nov 27;4(12):1960-76. doi: 10.3390/jcm4121952.

Claudin 1 in Breast Cancer: New Insights.

Author information

1
Department of Pathology, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E3P5, Canada. zhoub34@myumanitoba.ca.
2
Department of Pathology, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E3P5, Canada. moodie-a@webmail.uwinnipeg.ca.
3
Department of Pathology, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E3P5, Canada. anne.blanchard@umanitoba.ca.
4
Department of Physiology and Pathophysiology, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E0J9, Canada. anne.blanchard@umanitoba.ca.
5
Department of Biochemistry and Human Genetics, University of Manitoba, Winnipeg, MB R3E0J9, Canada. Etienne.leygue@umanitoba.ca.
6
Department of Pathology, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E3P5, Canada. Yvonne.myal@umanitoba.ca.
7
Department of Physiology and Pathophysiology, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E0J9, Canada. Yvonne.myal@umanitoba.ca.

Abstract

Claudin 1 is a small transmembrane protein responsible for maintaining the barrier function that exists between epithelial cells. A tight junction protein that regulates the paracellular transport of small ions across adjacent cells, claudin 1 maintains cellular polarity and plays a major role in cell-cell communication and epithelial cell homeostasis. Long considered to be a putative tumor suppressor in human breast cancer, new studies suggest a role much more complex. While most invasive breast cancers exhibit a down regulation or absence of claudin 1, some aggressive subtypes that exhibit high claudin 1 levels have now been described. Furthermore, a causal role for claudin 1 in breast cancer progression has recently been demonstrated in some breast cancer cell lines. In this review we highlight new insights into the role of claudin 1 in breast cancer, including its involvement in collective migration and epithelial mesenchymal transition (EMT).

KEYWORDS:

EMT; breast cancer; claudin 1; collective migration; interacting partners; “high claudin”

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