Special Issue "Epithelial-to-Mesenchymal Transition (EMT) in Cancer"
A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Therapeutics".
Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 10187
Special Issue Editor
Interests: cap-independent translation regulations; EMT; microRNA; eIF3e; ITAFs; heterogeneous ribonucleoproteins; diabetic nephropathy; cell signalling
Special Issue Information
Epithelial-to-mesenchymal transition (EMT) is an important event in embryonic development; the transition of epithelial cells to mesenchymal cells allows the formation of adult tissues and organs. Although EMT plays an important role during embryonic development, it is also aberrantly activated during cancer metastasis. EMT allows cancer cells to acquire migratory and invasive phenotypes that lead to the dissemination of tumor cells throughout the body. In addition, cancer cells that have undergone EMT have increased resistance to apoptosis, oncogene-induced senescence and exhibit increased resistance to chemotherapy. Almost 80% of malignant tumors are derived from the epithelial tissues of different organs such as the lung, colon, breast, pancreas, prostate, bladder, ovary, kidney, and liver. Moreover, cancer cells in early tumor states remain epithelial and have cohesive cell–cell junctions that inhibit their movements, and therefore they do not have migratory and/or invasive properties. Upon overexpression of mesenchymal specific factors, including fibronectin, vimentin, or neural cadherin (N-cadherin), the epithelial tumor cells exhibit mesenchymal features, such as mobility and invasion.
EMT is modulated at different levels of control, such as transcriptional control, epigenetic modifications, alternative splicing, translational regulation and microRNA-mediated gene silencing. Moreover, the cellular trans-differentiation from epithelial to mesenchymal states is regulated by many signaling pathways, of which the Ras-ERK, MAPK and TGF- β pathways are among the best characterized. These pathways trigger the activation of key transcription factors that serve as master regulators of cell–cell adhesion, cell polarity, and motility.
However, despite the intense research for last twenty years, our knowledge is very limited about how all these components regulate the transition. More research is necessary to understand the EMT mechanism and it will help us to identify appropriate drug target. This special issue will discuss the different aspect of EMT.
Dr. Amit Bera
Guest Editor
Manuscript Submission Information
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Keywords
- EMT
- migration
- invasion
- metastasis
- cancer progression