Abstract

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.

Highlights

  • Breast cancer is the most common cancer in women and ranks second among cancer deaths in women

  • These results suggested that a single cell may be undergoing into cluster characterize epithelial-mesenchymal transition (EMT) in circulating tumor cells (CTCs) from breast cancer patients [30]

  • A recent study from Xue et al showed that the mechanism of TGF-β-induced EMT in breast cancer cells is via the FOXM1 transactivation of Slug through the Smad pathway [55]

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Summary

Introduction

Breast cancer is the most common cancer in women and ranks second among cancer deaths in women. Med. 2016, 5, 13 metastasis suggests that a small subpopulation of cancer cells acquires cancer stem-like cell (CSCs) traits [12], exhibits mesenchymal cell characteristics, and migrates away from the primary tumor site and progresses to distant metastatic sites [13]. Demonstrating EMT in human cancer is complicated by the fact that most tissue samples obtained from human tumors were taken at various time points—either from primary or metastatic sites The tissues from these sites may have either not yet undergone EMT or undergone the reverse process of mesenchymal-to-epithelial transition (MET) [16,17,18,19], respectively. We will focus on discussing characteristics of EMT that may be evaluated in clinical samples for accessing EMT initiation and determining tumor progression in breast cancer

EMT and Its Plasticity Features
EMT and Breast Cancer Metastasis
EMT andEMT
Breast
EMT and Resistance to Treatment
Signaling Pathways Mediate EMT
TGF-β Signaling
Wnt Signaling
Notch Signaling
Interaction of Signaling Pathways on EMT
Epigenetics Regulation of EMT
DNA Methylation and Histone Modification in Regulation of EMT
MicroRNAs in Regulation of EMT
Epigenetic Therapies and EMT
Conclusions
Findings
Method
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