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Special Issue "Epithelial-Mesenchymal Transition (EMT) 2021"

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

Deadline for manuscript submissions: 30 June 2021.

Special Issue Editors

Prof. Dr. Monica Fedele
E-Mail Website
Guest Editor
CNR—Institute of Experimental Endocrinology and Oncology, 80131 Naples, Italy
Interests: molecular mechanisms of cancer cell transformation; PATZ1 in development and cancer; animal models; tumor biology
Special Issues and Collections in MDPI journals
Prof. Dr. Manfioletti Guidalberto
E-Mail Website
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
Special Issues and Collections in MDPI journals

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.

Prof. Dr. Monica Fedele
Prof. Dr. Manfioletti Guidalberto
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • EMT
  • Cancer progression
  • Embryogenesis
  • Tissue injury
  • Cell motility
  • Invasion
  • Metastasis
  • Stemness

Published Papers (1 paper)

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Open AccessArticle
Suppression of PGC-1α Drives Metabolic Dysfunction in TGFβ2-Induced EMT of Retinal Pigment Epithelial Cells
Int. J. Mol. Sci. 2021, 22(9), 4701; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094701 - 29 Apr 2021
Viewed by 225
PGC-1α, a key orchestrator of mitochondrial metabolism, plays a crucial role in governing the energetically demanding needs of retinal pigment epithelial cells (RPE). We previously showed that silencing PGC-1α induced RPE to undergo an epithelial-mesenchymal-transition (EMT). Here, we show that induction of EMT [...] Read more.
PGC-1α, a key orchestrator of mitochondrial metabolism, plays a crucial role in governing the energetically demanding needs of retinal pigment epithelial cells (RPE). We previously showed that silencing PGC-1α induced RPE to undergo an epithelial-mesenchymal-transition (EMT). Here, we show that induction of EMT in RPE using transforming growth factor-beta 2 (TGFβ2) suppressed PGC-1α expression. Correspondingly, TGFβ2 induced defects in mitochondrial network integrity with increased sphericity and fragmentation. TGFβ2 reduced expression of genes regulating mitochondrial dynamics, reduced citrate synthase activity and intracellular ATP content. High-resolution respirometry showed that TGFβ2 reduced mitochondrial OXPHOS levels consistent with reduced expression of NDUFB5. The reduced mitochondrial respiration was associated with a compensatory increase in glycolytic reserve, glucose uptake and gene expression of glycolytic enzymes (PFKFB3, PKM2, LDHA). Treatment with ZLN005, a selective small molecule activator of PGC-1α, blocked TGFβ2-induced upregulation of mesenchymal genes (αSMA, Snai1, CTGF, COL1A1) and TGFβ2-induced migration using the scratch wound assay. Our data show that EMT is accompanied by mitochondrial dysfunction and a metabolic shift towards reduced OXPHOS and increased glycolysis that may be driven by PGC-1α suppression. ZLN005 effectively blocks EMT in RPE and thus serves as a novel therapeutic avenue for treatment of subretinal fibrosis. Full article
(This article belongs to the Special Issue Epithelial-Mesenchymal Transition (EMT) 2021)
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