Cadherin Expression and EMT: A Focus on Gliomas
Cadherins are calcium-binding proteins with a pivotal role in cell adhesion and tissue homeostasis. The cadherin-dependent mechanisms of cell adhesion and migration are exploited by cancer cells, contributing to tumor invasiveness and dissemination. In particular, cadherin switch is a hallmark of ep...
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Published in | Biomedicines Vol. 9; no. 10; p. 1328 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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26.09.2021
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Abstract | Cadherins are calcium-binding proteins with a pivotal role in cell adhesion and tissue homeostasis. The cadherin-dependent mechanisms of cell adhesion and migration are exploited by cancer cells, contributing to tumor invasiveness and dissemination. In particular, cadherin switch is a hallmark of epithelial to mesenchymal transition, a complex development process vastly described in the progression of most epithelial cancers. This is characterized by drastic changes in cell polarity, adhesion, and motility, which lead from an E-cadherin positive differentiated epithelial state into a dedifferentiated mesenchymal-like state, prone to metastization and defined by N-cadherin expression. Although vastly explored in epithelial cancers, how these mechanisms contribute to the pathogenesis of other non-epithelial tumor types is poorly understood. Herein, the current knowledge on cadherin expression in normal development in parallel to tumor pathogenesis is reviewed, focusing on epithelial to mesenchymal transition. Emphasis is taken in the unascertained cadherin expression in CNS tumors, particularly in gliomas, where the potential contribution of an epithelial-to-mesenchymal-like process to glioma genesis and how this may be associated with changes in cadherin expression is discussed. |
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AbstractList | Cadherins are calcium-binding proteins with a pivotal role in cell adhesion and tissue homeostasis. The cadherin-dependent mechanisms of cell adhesion and migration are exploited by cancer cells, contributing to tumor invasiveness and dissemination. In particular, cadherin switch is a hallmark of epithelial to mesenchymal transition, a complex development process vastly described in the progression of most epithelial cancers. This is characterized by drastic changes in cell polarity, adhesion, and motility, which lead from an E-cadherin positive differentiated epithelial state into a dedifferentiated mesenchymal-like state, prone to metastization and defined by N-cadherin expression. Although vastly explored in epithelial cancers, how these mechanisms contribute to the pathogenesis of other non-epithelial tumor types is poorly understood. Herein, the current knowledge on cadherin expression in normal development in parallel to tumor pathogenesis is reviewed, focusing on epithelial to mesenchymal transition. Emphasis is taken in the unascertained cadherin expression in CNS tumors, particularly in gliomas, where the potential contribution of an epithelial-to-mesenchymal-like process to glioma genesis and how this may be associated with changes in cadherin expression is discussed. Cadherins are calcium-binding proteins with a pivotal role in cell adhesion and tissue homeostasis. The cadherin-dependent mechanisms of cell adhesion and migration are exploited by cancer cells, contributing to tumor invasiveness and dissemination. In particular, cadherin switch is a hallmark of epithelial to mesenchymal transition, a complex development process vastly described in the progression of most epithelial cancers. This is characterized by drastic changes in cell polarity, adhesion, and motility, which lead from an E-cadherin positive differentiated epithelial state into a dedifferentiated mesenchymal-like state, prone to metastization and defined by N-cadherin expression. Although vastly explored in epithelial cancers, how these mechanisms contribute to the pathogenesis of other non-epithelial tumor types is poorly understood. Herein, the current knowledge on cadherin expression in normal development in parallel to tumor pathogenesis is reviewed, focusing on epithelial to mesenchymal transition. Emphasis is taken in the unascertained cadherin expression in CNS tumors, particularly in gliomas, where the potential contribution of an epithelial-to-mesenchymal-like process to glioma genesis and how this may be associated with changes in cadherin expression is discussed.Cadherins are calcium-binding proteins with a pivotal role in cell adhesion and tissue homeostasis. The cadherin-dependent mechanisms of cell adhesion and migration are exploited by cancer cells, contributing to tumor invasiveness and dissemination. In particular, cadherin switch is a hallmark of epithelial to mesenchymal transition, a complex development process vastly described in the progression of most epithelial cancers. This is characterized by drastic changes in cell polarity, adhesion, and motility, which lead from an E-cadherin positive differentiated epithelial state into a dedifferentiated mesenchymal-like state, prone to metastization and defined by N-cadherin expression. Although vastly explored in epithelial cancers, how these mechanisms contribute to the pathogenesis of other non-epithelial tumor types is poorly understood. Herein, the current knowledge on cadherin expression in normal development in parallel to tumor pathogenesis is reviewed, focusing on epithelial to mesenchymal transition. Emphasis is taken in the unascertained cadherin expression in CNS tumors, particularly in gliomas, where the potential contribution of an epithelial-to-mesenchymal-like process to glioma genesis and how this may be associated with changes in cadherin expression is discussed. |
Author | Castro, Diogo S. Reis, Joaquim Ribeiro, Ana Sofia Noronha, Carolina Taipa, Ricardo Paredes, Joana Faria, Cláudia |
AuthorAffiliation | 2 Cancer Metastasis Group, i3S—Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal; aribeiro@ipatimup.pt 5 Unit for Multidisciplinary Research in Biomedicine (UMIB), Institute of Biomedical Sciences Abel Salazar, University of Porto, 4050-313 Porto, Portugal 3 Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal 8 Neurosurgery Department, Hospital de Santa Maria, Centro Hospitalar Universitario Lisboa Norte, 1649-028 Lisboa, Portugal; claudiamfaria@gmail.com 9 IMM—Instituto de Medicina Molecular Joao Lobo Antunes, Universidade de Lisboa, 1649-028 Lisboa, Portugal 6 Stem Cells & Neurogenesis Group, i3S—Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal; diogo.castro@i3s.up.pt 1 Neurosurgery Department, Hospital de Santo António, Centro Hospitalar Universitario do Porto, 4099-001 Porto, Portugal; cnoronha@ipatimup.pt (C.N.); jlreis@icbas.up.pt (J.R.) 4 Neuropathology Unit, Hospital de Santo Antó |
AuthorAffiliation_xml | – name: 6 Stem Cells & Neurogenesis Group, i3S—Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal; diogo.castro@i3s.up.pt – name: 1 Neurosurgery Department, Hospital de Santo António, Centro Hospitalar Universitario do Porto, 4099-001 Porto, Portugal; cnoronha@ipatimup.pt (C.N.); jlreis@icbas.up.pt (J.R.) – name: 9 IMM—Instituto de Medicina Molecular Joao Lobo Antunes, Universidade de Lisboa, 1649-028 Lisboa, Portugal – name: 4 Neuropathology Unit, Hospital de Santo António, Centro Hospitalar Universitario do Porto, 4099-001 Porto, Portugal; rtaipa.neuropat@chporto.min-saude.pt – name: 8 Neurosurgery Department, Hospital de Santa Maria, Centro Hospitalar Universitario Lisboa Norte, 1649-028 Lisboa, Portugal; claudiamfaria@gmail.com – name: 2 Cancer Metastasis Group, i3S—Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal; aribeiro@ipatimup.pt – name: 3 Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal – name: 5 Unit for Multidisciplinary Research in Biomedicine (UMIB), Institute of Biomedical Sciences Abel Salazar, University of Porto, 4050-313 Porto, Portugal – name: 7 Anatomy Department, Institute of Biomedical Sciences Abel Salazar, University of Porto, 4050-313 Porto, Portugal |
Author_xml | – sequence: 1 givenname: Carolina surname: Noronha fullname: Noronha, Carolina – sequence: 2 givenname: Ana Sofia orcidid: 0000-0002-9698-9233 surname: Ribeiro fullname: Ribeiro, Ana Sofia – sequence: 3 givenname: Ricardo orcidid: 0000-0002-9260-0227 surname: Taipa fullname: Taipa, Ricardo – sequence: 4 givenname: Diogo S. orcidid: 0000-0001-8178-9565 surname: Castro fullname: Castro, Diogo S. – sequence: 5 givenname: Joaquim surname: Reis fullname: Reis, Joaquim – sequence: 6 givenname: Cláudia surname: Faria fullname: Faria, Cláudia – sequence: 7 givenname: Joana orcidid: 0000-0002-1076-1343 surname: Paredes fullname: Paredes, Joana |
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