Context-dependent EMT programs in cancer metastasis

Epithelial–mesenchymal transition (EMT) is a developmental process whereby stationary, adherent cells acquire the ability to migrate. EMT is critical for dramatic cellular movements during embryogenesis; however, tumor cells can reactivate EMT programs, which increases their aggressiveness. In addit...

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Bibliographic Details
Published inThe Journal of experimental medicine Vol. 216; no. 5; pp. 1016 - 1026
Main Authors Aiello, Nicole M., Kang, Yibin
Format Journal Article
LanguageEnglish
Published United States Rockefeller University Press 06.05.2019
Subjects
Animals
Biomarkers, Tumor
Cell Movement
Cell Plasticity
Epithelial Cells - metabolism
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
Humans
Mesenchymal Stem Cells - metabolism
Mice
Neoplasm Metastasis
Neoplasms - pathology
Reviews
Online AccessGet full text

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Abstract Epithelial–mesenchymal transition (EMT) is a developmental process whereby stationary, adherent cells acquire the ability to migrate. EMT is critical for dramatic cellular movements during embryogenesis; however, tumor cells can reactivate EMT programs, which increases their aggressiveness. In addition to motility, EMT is associated with enhanced stem cell properties and drug resistance; thus it can drive metastasis, tumor recurrence, and therapy resistance in the context of cancer. However, the precise requirements for EMT in metastasis have not been fully delineated, with different tumor types relying on discrete EMT effectors. Most tumor cells do not undergo a full EMT, but rather adopt some qualities of mesenchymal cells and maintain some epithelial characteristics. Emerging evidence suggests that partial EMT can drive distinct migratory properties and enhance the epithelial-mesenchymal plasticity of cancer cells as well as cell fate plasticity. This review discusses the diverse regulatory mechanisms and functional consequences of EMT, with an emphasis on the importance of partial EMT.
AbstractList Epithelial–mesenchymal transition (EMT) is a developmental process whereby stationary, adherent cells acquire the ability to migrate. EMT is critical for dramatic cellular movements during embryogenesis; however, tumor cells can reactivate EMT programs, which increases their aggressiveness. In addition to motility, EMT is associated with enhanced stem cell properties and drug resistance; thus it can drive metastasis, tumor recurrence, and therapy resistance in the context of cancer. However, the precise requirements for EMT in metastasis have not been fully delineated, with different tumor types relying on discrete EMT effectors. Most tumor cells do not undergo a full EMT, but rather adopt some qualities of mesenchymal cells and maintain some epithelial characteristics. Emerging evidence suggests that partial EMT can drive distinct migratory properties and enhance the epithelial-mesenchymal plasticity of cancer cells as well as cell fate plasticity. This review discusses the diverse regulatory mechanisms and functional consequences of EMT, with an emphasis on the importance of partial EMT.
In this review, Aiello and Kang discuss the molecular mechanisms, regulatory networks, and functional consequences of epithelial–mesenchymal transition (EMT) in the context of cancer metastasis, with a particular focus on partial EMT and cellular plasticity. Epithelial–mesenchymal transition (EMT) is a developmental process whereby stationary, adherent cells acquire the ability to migrate. EMT is critical for dramatic cellular movements during embryogenesis; however, tumor cells can reactivate EMT programs, which increases their aggressiveness. In addition to motility, EMT is associated with enhanced stem cell properties and drug resistance; thus it can drive metastasis, tumor recurrence, and therapy resistance in the context of cancer. However, the precise requirements for EMT in metastasis have not been fully delineated, with different tumor types relying on discrete EMT effectors. Most tumor cells do not undergo a full EMT, but rather adopt some qualities of mesenchymal cells and maintain some epithelial characteristics. Emerging evidence suggests that partial EMT can drive distinct migratory properties and enhance the epithelial-mesenchymal plasticity of cancer cells as well as cell fate plasticity. This review discusses the diverse regulatory mechanisms and functional consequences of EMT, with an emphasis on the importance of partial EMT.
Epithelial-mesenchymal transition (EMT) is a developmental process whereby stationary, adherent cells acquire the ability to migrate. EMT is critical for dramatic cellular movements during embryogenesis; however, tumor cells can reactivate EMT programs, which increases their aggressiveness. In addition to motility, EMT is associated with enhanced stem cell properties and drug resistance; thus it can drive metastasis, tumor recurrence, and therapy resistance in the context of cancer. However, the precise requirements for EMT in metastasis have not been fully delineated, with different tumor types relying on discrete EMT effectors. Most tumor cells do not undergo a full EMT, but rather adopt some qualities of mesenchymal cells and maintain some epithelial characteristics. Emerging evidence suggests that partial EMT can drive distinct migratory properties and enhance the epithelial-mesenchymal plasticity of cancer cells as well as cell fate plasticity. This review discusses the diverse regulatory mechanisms and functional consequences of EMT, with an emphasis on the importance of partial EMT.Epithelial-mesenchymal transition (EMT) is a developmental process whereby stationary, adherent cells acquire the ability to migrate. EMT is critical for dramatic cellular movements during embryogenesis; however, tumor cells can reactivate EMT programs, which increases their aggressiveness. In addition to motility, EMT is associated with enhanced stem cell properties and drug resistance; thus it can drive metastasis, tumor recurrence, and therapy resistance in the context of cancer. However, the precise requirements for EMT in metastasis have not been fully delineated, with different tumor types relying on discrete EMT effectors. Most tumor cells do not undergo a full EMT, but rather adopt some qualities of mesenchymal cells and maintain some epithelial characteristics. Emerging evidence suggests that partial EMT can drive distinct migratory properties and enhance the epithelial-mesenchymal plasticity of cancer cells as well as cell fate plasticity. This review discusses the diverse regulatory mechanisms and functional consequences of EMT, with an emphasis on the importance of partial EMT.
Author Aiello, Nicole M.
Kang, Yibin
AuthorAffiliation Department of Molecular Biology, Princeton University, Princeton, NJ
AuthorAffiliation_xml – name: Department of Molecular Biology, Princeton University, Princeton, NJ
Author_xml – sequence: 1
  givenname: Nicole M.
  surname: Aiello
  fullname: Aiello, Nicole M.
– sequence: 2
  givenname: Yibin
  orcidid: 0000-0002-1626-6730
  surname: Kang
  fullname: Kang, Yibin
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30975895$$D View this record in MEDLINE/PubMed
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Snippet Epithelial–mesenchymal transition (EMT) is a developmental process whereby stationary, adherent cells acquire the ability to migrate. EMT is critical for...
Epithelial-mesenchymal transition (EMT) is a developmental process whereby stationary, adherent cells acquire the ability to migrate. EMT is critical for...
In this review, Aiello and Kang discuss the molecular mechanisms, regulatory networks, and functional consequences of epithelial–mesenchymal transition (EMT)...
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StartPage 1016
SubjectTerms Animals
Biomarkers, Tumor
Cell Movement
Cell Plasticity
Epithelial Cells - metabolism
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
Humans
Mesenchymal Stem Cells - metabolism
Mice
Neoplasm Metastasis
Neoplasms - pathology
Reviews
Title Context-dependent EMT programs in cancer metastasis
URI https://www.ncbi.nlm.nih.gov/pubmed/30975895
https://www.proquest.com/docview/2209600841
https://pubmed.ncbi.nlm.nih.gov/PMC6504222
Volume 216
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