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Epithelial-Mesenchymal Transition (EMT) and Regulation of EMT Factors by Steroid Nuclear Receptors in Breast Cancer: A Review and in Silico Investigation
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Epithelial-Mesenchymal Transition and Breast Cancer

1
Division of Cancer Research and Training, Department of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA
2
Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Jane Grant-Kels
J. Clin. Med. 2016, 5(2), 13; https://doi.org/10.3390/jcm5020013
Received: 1 December 2015 / Revised: 11 January 2016 / Accepted: 19 January 2016 / Published: 26 January 2016
(This article belongs to the Special Issue Epithelial-Mesenchymal Transition)
Breast cancer is the most common cancer in women and distant site metastasis is the main cause of death in breast cancer patients. There is increasing evidence supporting the role of epithelial-mesenchymal transition (EMT) in tumor cell progression, invasion, and metastasis. During the process of EMT, epithelial cancer cells acquire molecular alternations that facilitate the loss of epithelial features and gain of mesenchymal phenotype. Such transformation promotes cancer cell migration and invasion. Moreover, emerging evidence suggests that EMT is associated with the increased enrichment of cancer stem-like cells (CSCs) and these CSCs display mesenchymal characteristics that are resistant to chemotherapy and target therapy. However, the clinical relevance of EMT in human cancer is still under debate. This review will provide an overview of current evidence of EMT from studies using clinical human breast cancer tissues and its associated challenges. View Full-Text
Keywords: breast cancer; epithelial cells; metastasis breast cancer; epithelial cells; metastasis
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Wu, Y.; Sarkissyan, M.; Vadgama, J.V. Epithelial-Mesenchymal Transition and Breast Cancer. J. Clin. Med. 2016, 5, 13.

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