Special Issue "Epithelial-Mesenchymal Transition (EMT)"
Deadline for manuscript submissions: closed (31 March 2019)
Prof. Dr. Monica Fedele
CNR—Institute of Experimental Endocrinology and Oncology, 80131 Naples, Italy
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Interests: PATZ1; HMGA; chromatin; gene regulation; cancer; biomarkers; animal models; cancer cells; transgenic mice; knockout mice; breast cancer; glioblastoma; thyroid cancer; pituitary adenomas; EMT; cancer stem cells
Prof. G. Manfioletti
Department of Life Science, Università degli Studi di Trieste, Trieste, Italy
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Interests: high mobility group A (HMGA) proteins; chromatin; regulation of gene expression; protein-protein interactions; post-translational modifications (PTMs); epithelial-mesenchymal transition; cancer; tumor microenvironment; development
The Epithelial-Mesenchymal transition (EMT), a biological process that allows an epithelial cell to assume a mesenchymal phenotype, including enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, stem-like features, and increased production of ECM components, occur during specific steps of embryogenesis and organ development leading to final differentiation. Due to its plasticity and reversibility, terminally differentiated epithelium can transdifferentiate and change its phenotype through EMT. This process can also be activated in pathological situation, such as tissue injury and repair or neoplastic transformation. Indeed, it is now well recognized that EMT constitutes the first step for the invasiveness and metastatic dissemination of epithelial cancer cells. Moreover, acquisition of mesenchymal features in non-epithelial cancers, such as glioblastomas, has been associated with invasiveness and aggressiveness of the tumor, together with a worse prognosis of the patients.
The EMT program is initiated by different molecular processes, including activation of transcriptional factors, expression of specific cell-surface proteins, reorganization and expression of cytoskeletal proteins, production of ECM-degrading enzymes, and changes in the expression of microRNAs. There are both endogenous cell autonomous and exogenous non-cell autonomous signals occurring in the process, including pathways orchestrated by TGF-b, Notch, Wnt, Hedgehog, and receptor tyrosine kinases, as well as the urokinase plasminogen activator system, the secretome of associated fibroblasts, macrophages, cancer stem cells and cancer cells, and exosomes with their cargo of microRNAs.
However, despite the intense investigation of the last years, relatively little is known about how all these components are integrated and participate in the same process, and how the mesenchymal state is maintained. Deep knowledge of these aspects will help to design potential therapeutic approaches that could exploit the plasticity of this process to reverse the metastatic phenotype of many cancers. Papers related to any aspect of EMT will be considered for this Special issue.
Prof. Dr. Monica Fedele
Prof. Dr. Guidalberto Manfioletti
Manuscript Submission Information
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- cancer progression
- tissue injury
- cell motility