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      Endothelial-to-Mesenchymal Transition (EndoMT): Roles in Tumorigenesis, Metastatic Extravasation and Therapy Resistance

      review-article
      Author(s): 1 , 1 , 2 , , 1 ,
      Publication date (Electronic):
      Journal: Journal of Oncology
      Publisher: Hindawi

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          Abstract

          Cancer cells evolve in a very complex tumor microenvironment, composed of several cell types, among which the endothelial cells are the major actors of the tumor angiogenesis. Today, these cells are also characterized for their plasticity, as endothelial cells have demonstrated their potential to modify their phenotype to differentiate into mesenchymal cells through the endothelial-to-mesenchymal transition (EndoMT). This cellular plasticity is mediated by various stimuli including transforming growth factor- β (TGF- β) and is modulated dependently of experimental conditions. Recently, emerging evidences have shown that EndoMT is involved in the development and dissemination of cancer and also in cancer cell to escape from therapeutic treatment. In this review, we summarize current updates on EndoMT and its main induction pathways. In addition, we discuss the role of EndoMT in tumorigenesis, metastasis, and its potential implication in cancer therapy resistance.

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          TGF-β-Mediated Epithelial-Mesenchymal Transition and Cancer Metastasis

          Yang Hao, David Baker, Peter ten Dijke (2019)
          Transforming growth factor β (TGF-β) is a secreted cytokine that regulates cell proliferation, migration, and the differentiation of a plethora of different cell types. Consistent with these findings, TGF-β plays a key role in controlling embryogenic development, inflammation, and tissue repair, as well as in maintaining adult tissue homeostasis. TGF-β elicits a broad range of context-dependent cellular responses, and consequently, alterations in TGF-β signaling have been implicated in many diseases, including cancer. During the early stages of tumorigenesis, TGF-β acts as a tumor suppressor by inducing cytostasis and the apoptosis of normal and premalignant cells. However, at later stages, when cancer cells have acquired oncogenic mutations and/or have lost tumor suppressor gene function, cells are resistant to TGF-β-induced growth arrest, and TGF-β functions as a tumor promotor by stimulating tumor cells to undergo the so-called epithelial-mesenchymal transition (EMT). The latter leads to metastasis and chemotherapy resistance. TGF-β further supports cancer growth and progression by activating tumor angiogenesis and cancer-associated fibroblasts and enabling the tumor to evade inhibitory immune responses. In this review, we will consider the role of TGF-β signaling in cell cycle arrest, apoptosis, EMT and cancer cell metastasis. In particular, we will highlight recent insights into the multistep and dynamically controlled process of TGF-β-induced EMT and the functions of miRNAs and long noncoding RNAs in this process. Finally, we will discuss how these new mechanistic insights might be exploited to develop novel therapeutic interventions.
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            Fibroblasts in kidney fibrosis emerge via endothelial-to-mesenchymal transition.

            Elisabeth M. Zeisberg, Scott Potenta, Hikaru Sugimoto … (2008)
            Fibroblasts are key mediators of fibrosis in the kidney and other organs, but their origin during fibrosis is still not completely clear. Activated fibroblasts likely arise from resident quiescent fibroblasts via epithelial-to-mesenchymal transition and from the bone marrow. Here, we demonstrate that endothelial cells also contribute to the emergence of fibroblasts during kidney fibrosis via the process of endothelial-to-mesenchymal transition (EndMT). We examined the contribution of EndMT to renal fibrosis in three mouse models of chronic kidney disease: (1) Unilateral ureteral obstructive nephropathy, (2) streptozotocin-induced diabetic nephropathy, and (3) a model of Alport renal disease. Approximately 30 to 50% of fibroblasts coexpressed the endothelial marker CD31 and markers of fibroblasts and myofibroblasts such as fibroblast specific protein-1 and alpha-smooth muscle actin. Endothelial lineage tracing using Tie2-Cre;R26R-stop-EYFP transgenic mice further confirmed the presence of EndMT-derived fibroblasts. Collectively, our results demonstrate that EndMT contributes to the accumulation of activated fibroblasts and myofibroblasts in kidney fibrosis and suggest that targeting EndMT might have therapeutic potential.
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              The Notch signalling system: recent insights into the complexity of a conserved pathway.

              K G Guruharsha, Mark Kankel, Spyros Artavanis-Tsakonas (2012)
              Notch signalling links the fate of one cell to that of an immediate neighbour and consequently controls differentiation, proliferation and apoptotic events in multiple metazoan tissues. Perturbations in this pathway activity have been linked to several human genetic disorders and cancers. Recent genome-scale studies in Drosophila melanogaster have revealed an extraordinarily complex network of genes that can affect Notch activity. This highly interconnected network contrasts our traditional view of the Notch pathway as a simple linear sequence of events. Although we now have an unprecedented insight into the way in which such a fundamental signalling mechanism is controlled by the genome, we are faced with serious challenges in analysing the underlying molecular mechanisms of Notch signal control.
              Article 0 comments Cited 254 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Isabelle Corre:
                ORCID: https://orcid.org/0000-0001-6444-1145
                Nicolas Clere:
                ORCID: https://orcid.org/0000-0002-6008-597X
                Journal
                Journal ID (nlm-ta): J Oncol
                Journal ID (iso-abbrev): J Oncol
                Journal ID (publisher-id): JO
                Title: Journal of Oncology
                Publisher: Hindawi
                ISSN (Print): 1687-8450
                ISSN (Electronic): 1687-8469
                Publication date Collection: 2019
                Publication date (Electronic): 1 August 2019
                Volume: 2019
                Electronic Location Identifier: 8361945
                Affiliations
                1Micro & Nanomédecines Translationnelles-MINT, Univ Angers, INSERM U1066, CNRS UMR 6021, Angers, France
                2Sarcomes Osseux et Remodelage des Tissus Calcifiés Phy-OS, Université de Nantes INSERM UMR U1238, Faculté de Médecine, F-44035 Nantes, France
                Author notes

                Academic Editor: Daniele Vergara

                Author information
                https://orcid.org/0000-0001-6444-1145
                https://orcid.org/0000-0002-6008-597X
                Article
                DOI: 10.1155/2019/8361945
                PMC ID: 6701373
                PubMed ID: 31467544
                SO-VID: fc4e9119-ffce-426e-af86-d0b81e721428
                Copyright © Copyright © 2019 Valentin Platel et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 4 April 2019
                Date revision received : 20 June 2019
                Date accepted : 1 July 2019
                Funding
                Funded by: Région Pays de la Loire
                Funded by: Comité départemental du Maine et Loire de la Ligue contre le Cancer
                Funded by: Comité départemental de Loire Atlantique de la Ligue contre le Cancer
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Oncology & Radiotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy

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