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Review
. 2016 Jan 26;5(2):13.
doi: 10.3390/jcm5020013.

Epithelial-Mesenchymal Transition and Breast Cancer

Yanyuan Wu  1   2 , Marianna Sarkissyan  3 , Jaydutt V Vadgama  4   5
Affiliations
Review

Epithelial-Mesenchymal Transition and Breast Cancer

Yanyuan Wu et al. J Clin Med. .

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.

Keywords: breast cancer; epithelial cells; metastasis.

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Figures

Figure 1
Figure 1
Schematic of the epithelial to mesenchymal transition (EMT). This process results in a transformation and transition of polarized epithelial cells toward mobile mesenchymal cells. Expression of cytokeratins is a feature of epithelial cells. The increased expression of Snail, Slug, Twist, fibronectin and Vimentin is common in mesenchymal cells. The E-cadherin to N-cadherin switch indicates epithelial cells are progressing through EMT.
Figure 2
Figure 2
Breast CSCs display a cellular plasticity that allows them to transition between EMT and MET states. Hypothetical models show the characteristics of two different states of BCSCs as suggested by Liu et al. [36].
See this image and copyright information in PMC

References

    1. Perou C.M., Sorlie T., Eisen M.B., van de Rijn M., Jeffrey S.S., Rees C.A., Pollack J.R., Ross D.T., Johnsen H., Akslen L.A., et al. Molecular portraits of human breast tumors. Nature. 2000;406:747–752. doi: 10.1038/35021093. - DOI - PubMed
    1. Sorlie T., Perou C.M., Tibshirani R., Aas T., Geisler S., Johnsen H., Hastie T., Eisen M.B., van de Rijn M., Jeffrey S.S., et al. Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications. Proc. Natl. Acad. Sci. USA. 2001;98:10869–10874. doi: 10.1073/pnas.191367098. - DOI - PMC - PubMed
    1. Sorlie T., Tibshirani R., Parker J., Hastie T., Marron J.S., Nobel A., Deng S., Johnsen H., Pesich R., Geisler S., et al. Repeated observation of breast tumor subtypes in independent gene expression data sets. Proc. Natl. Acad. Sci. USA. 2003;100:8418–8423. doi: 10.1073/pnas.0932692100. - DOI - PMC - PubMed
    1. Sotiriou C., Neo S.Y., McShane L.M., Korn E.L., Long P.M., Jazaeri A., Martiat P., Fox S.B., Harris A.L., Liu E.T. Breast cancer classification and prognosis based on gene expression profiles from a population-based study. Proc. Natl. Acad. Sci. USA. 2003;100:10393–10398. doi: 10.1073/pnas.1732912100. - DOI - PMC - PubMed
    1. Sethi S., Sarkar F.H., Ahmed Q., Bandyopadhyay S., Nahleh Z.A., Semaan A., Sarkr W., Munkarah A., Ali-Fehmi R. Molecular markers of epithelial-to mesenchymal transition are associated with tumor aggressiveness in breast carcinoma. Translational. Oncol. 2011;4:222–226. doi: 10.1593/tlo.10244. - DOI - PMC - PubMed