Abstract
Epithelial-to-mesenchymal transition (EMT) is a fundamental cellular phenomenon that plays an intrinsic role in development, tissue repair, and cancer progression. EMT is tightly regulated by transcription factors that alter gene expression to promote epithelial to mesenchymal phenotype. EMT is also regulated by a diverse array of cytokines and growth factors whose activities are deregulated during malignancy. EMT enables tumor cells to exist in various intermediate states along the epithelial-mesenchymal phenotypic axis that transit from cancer stem cells (CSCs) to circulating tumor cells (CTCs). Recent studies have revealed the importance of CSCs in tumor promotion, invasion and metastasis. The relapsed tumors encompass CSCs which are resistant to radiotherapy and chemotherapy. In this review, we have summarized our current understanding of the molecular mechanisms that regulate EMT induced CSC phenotype. We have highlighted studies implicating the function of TGF-�, Wnt, and Notch regulated non-coding RNAs in driving EMT promoting CSC self-renewal. Finally, we discuss how the EMT and CSCs cause drug resistance with the hope to overcome such resistance as a possible approach for cancer treatment.
Highlights
Epithelial-mesenchymal transition is a cellular phenomenon that allows a stationary polarized epithelial cell to undergo various morphological changes to assume a migratory, invasive mesenchymal cell phenotype
Cancer metastasis is driven by epithelial to mesenchymal transition (EMT) mainly by conversion of cancer cells to cancer stem cells (CSCs), which are capable of traversing tissue boundaries, entering into the blood vessels, localizing and growing in other tissues to form metastatic foci
We focus on EMT, plasticity, circulating tumor cells (CTCs), cancer stemness with an emphasis on the the role of cellular signaling in development of EMT in head and neck squamous cell carcinoma (HNSCC) and breast cancers (BC)
Summary
Epithelial-mesenchymal transition is a cellular phenomenon that allows a stationary polarized epithelial cell to undergo various morphological changes to assume a migratory, invasive mesenchymal cell phenotype. The process known as epithelial to mesenchymal transition (EMT) is an intrinsic cellular phenomenon reminiscent of embryonic development and tissue repair, which occurs during diverse disease processes including cancer invasion, organ fibrosis [2]. The activation of EMT-TFs occurs in response to various signaling pathways such as Transforming Growth Factor β (TGF-β), Wnt and Notch. These extracellular signals activate the intracellular kinase cascades which induce the expression of EMT-TFs. EMT and mesenchymal to epithelial transition (MET) which involves the conversion of mesenchymal cells to epithelial cells are consistent with the idea of cell plasticity. We focus on EMT, plasticity, CTCs, cancer stemness with an emphasis on the the role of cellular signaling in development of EMT in head and neck squamous cell carcinoma (HNSCC) and breast cancers (BC)
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