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Claudin 1 in Breast Cancer: New Insights

1
Department of Pathology, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E3P5, Canada
2
Department of Physiology and Pathophysiology, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E0J9, Canada
3
Department of Biochemistry and Human Genetics, University of Manitoba, Winnipeg, MB R3E0J9, Canada
*
Author to whom correspondence should be addressed.
Academic Editor: Jane Grant-Kels
J. Clin. Med. 2015, 4(12), 1960-1976; https://doi.org/10.3390/jcm4121952
Received: 1 October 2015 / Revised: 9 November 2015 / Accepted: 14 November 2015 / Published: 27 November 2015
(This article belongs to the Special Issue Epithelial-Mesenchymal Transition)
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). View Full-Text
Keywords: claudin 1; breast cancer; EMT; “high claudin”; collective migration; interacting partners claudin 1; breast cancer; EMT; “high claudin”; collective migration; interacting partners
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MDPI and ACS Style

Zhou, B.; Moodie, A.; Blanchard, A.A.A.; Leygue, E.; Myal, Y. Claudin 1 in Breast Cancer: New Insights. J. Clin. Med. 2015, 4, 1960-1976.

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