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Epithelial-Mesenchymal Transition (EMT) 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 3384

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Guest Editor

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Guest Editor
Department of Life Sciences, University of Trieste, 34127 Trieste, Italy
Interests: high mobility group A (HMGA) proteins; chromatin; regulation of gene expression; protein–protein interactions; post-translational modifications (PTMs); epithelial–mesenchymal transition; proteomics; tumor microenvironment; breast cancer; metastasis
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Special Issue Information

Dear Colleagues,

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, occurs 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 a 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 noncell 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 intense investigation in recent 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.

Dr. Monica Fedele
Prof. Guidalberto Manfioletti
Guest Editors


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Keywords

  • EMT
  • cancer progression
  • embryogenesis
  • tissue injury
  • cell motility
  • invasion
  • metastasis
  • stemness

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Published Papers (1 paper)

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16 pages, 5901 KiB  
Article
Fluidity of Poly (ε-Caprolactone)-Based Material Induces Epithelial-to-Mesenchymal Transition
by Sharmy Saimon Mano, Koichiro Uto and Mitsuhiro Ebara
Int. J. Mol. Sci. 2020, 21(5), 1757; https://doi.org/10.3390/ijms21051757 - 4 Mar 2020
Cited by 3 | Viewed by 2820
Abstract
Background: We propose the potential studies on material fluidity to induce epithelial to mesenchymal transition (EMT) in MCF-7 cells. In this study, we examined for the first time the effect of material fluidity on EMT using poly(ε-caprolactone-co-D,L-lactide) [...] Read more.
Background: We propose the potential studies on material fluidity to induce epithelial to mesenchymal transition (EMT) in MCF-7 cells. In this study, we examined for the first time the effect of material fluidity on EMT using poly(ε-caprolactone-co-D,L-lactide) (P(CL-co-DLLA)) with tunable elasticity and fluidity. Methods: The fluidity was altered by chemically crosslinking the polymer networks. The crosslinked P(CL-co-DLLA) substrate showed a solid-like property with a stiffness of 261 kPa, while the non-crosslinked P(CL-co-DLLA) substrate of 100 units (high fluidity) and 500 units (low fluidity) existed in a quasi-liquid state with loss modulus of 33 kPa and 30.8 kPa, respectively, and storage modulus of 10.8 kPa and 20.1 kPa, respectively. Results: We observed that MCF-7 cells on low fluidic substrates decreased the expression of E-cadherin, an epithelial marker, and increased expression of vimentin, a mesenchymal marker. This showed that the cells lose their epithelial phenotype and gain a mesenchymal property. On the other hand, MCF-7 cells on high fluidic substrates maintained their epithelial phenotype, suggesting that the cells did not undergo EMT. Conclusion: Considering these results as the fundamental information for material fluidity induced EMT, our system could be used to regulate the degree of EMT by turning the fluidity of the material. Full article
(This article belongs to the Special Issue Epithelial-Mesenchymal Transition (EMT) 2.0)
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