Abstract
The epithelial to mesenchymal transition (EMT) is a cellular program that is involved in embryonic development; wound healing, but also in tumorigenesis. Breast carcinoma (BC) is the most common cancer in women worldwide, and the majority of deaths (90%) are caused by invasion and metastasis. The EMT plays an important role in invasion and subsequent metastasis. Several distinct biological events integrate a cascade that leads not only to a change from an epithelial to mesenchymal phenotype, but allows for detachment, migration, invasion and ultimately, colonization of a second site. Understanding the biological intricacies of the EMT may provide important insights that lead to the development of therapeutic targets in pre-invasive and invasive breast cancer, and could be used as biomarkers identifying tumor subsets with greater chances of recurrence, metastasis and therapeutic resistance leading to death.
Highlights
The epithelial to mesenchymal transition (EMT) is a complex program in which epithelial cells acquire a mesenchymal phenotype and motility through a cascade of biological events
The EMT is believed to be a critical step in the progression of cancers from both the pre-invasive to invasive state, and from organ confined to metastatic disease [4], though there is evidence to show that the EMT is not an obligate step to metastasis, as discussed further in this review
Micalizzi et al highlighted the findings that triple-negative breast cancer displays up-regulation of EMT markers and overexpression of proteins involved in extracellular matrix remodeling and invasion (SPARC, laminin, and fascin); together with reduced expression of epithelial markers (E-cadherin and cytokeratins), which preferentially occur in breast tumors with the “basal-like phenotype”, linking EMT with the latter [3]
Summary
The epithelial to mesenchymal transition (EMT) is a complex program in which epithelial cells acquire a mesenchymal phenotype and motility through a cascade of biological events. The master regulators of the EMT include many pathways, the primary mediators of the EMT include signaling through TGF-β, Notch and Wnt; but are influenced by the effects of the tumor microenvironment such as hypoxia as well as the differential expression of microRNAs (miRNAs) (Figure 1) [5,6] Common to all these pathways are the convergence on the transcriptional. (miRNAs) (Figure 1) [5,6] Common to all these pathways are the convergence on the transcriptional factors SNAI (Snail), Zeb and Twist, whose differential expression in cancers has been shown to lead. Taylor et al [6] In this brief review, we will discuss the roles of these pathways in the EMT program as it pertains to its contribution to the progression of breast cancer and offer insight to the potential for biomarker discovery and therapeutic intervention
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