Epithelial-Mesenchymal Transition (EMT) as a Therapeutic Target.


Journal

Cells, tissues, organs
ISSN: 1422-6421
Titre abrégé: Cells Tissues Organs
Pays: Switzerland
ID NLM: 100883360

Informations de publication

Date de publication:
2022
Historique:
received: 15 06 2020
accepted: 11 10 2020
pubmed: 6 1 2021
medline: 3 5 2022
entrez: 5 1 2021
Statut: ppublish

Résumé

Metastasis is the spread of cancer cells from the primary tumour to distant sites and organs throughout the body. It is the primary cause of cancer morbidity and mortality, and is estimated to account for 90% of cancer-related deaths. During the initial steps of the metastatic cascade, epithelial cancer cells undergo an epithelial-mesenchymal transition (EMT), and as a result become migratory and invasive mesenchymal-like cells while acquiring cancer stem cell properties and therapy resistance. As EMT is involved in such a broad range of processes associated with malignant transformation, it has become an increasingly interesting target for the development of novel therapeutic strategies. Anti-EMT therapeutic strategies could potentially not only prevent the invasion and dissemination of cancer cells, and as such prevent the formation of metastatic lesions, but also attenuate cancer stemness and increase the effectiveness of more classical chemotherapeutics. In this review, we give an overview about the pros and cons of therapies targeting EMT and discuss some already existing candidate drug targets and high-throughput screening tools to identify novel anti-EMT compounds.

Identifiants

pubmed: 33401271
pii: 000512218
doi: 10.1159/000512218
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

157-182

Subventions

Organisme : Wellcome Trust
ID : 204615/Z/16/Z
Pays : United Kingdom

Informations de copyright

© 2021 S. Karger AG, Basel.

Auteurs

Sven Jonckheere (S)

Cancer Research Institute Ghent (CRIG), Ghent University, Ghent, Belgium.
Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.

Jamie Adams (J)

Department of Biomedical Science, The University of Sheffield, Sheffield, United Kingdom.

Dominic De Groote (D)

Cancer Research Institute Ghent (CRIG), Ghent University, Ghent, Belgium.

Kyra Campbell (K)

Department of Biomedical Science, The University of Sheffield, Sheffield, United Kingdom.

Geert Berx (G)

Cancer Research Institute Ghent (CRIG), Ghent University, Ghent, Belgium.
Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.

Steven Goossens (S)

Cancer Research Institute Ghent (CRIG), Ghent University, Ghent, Belgium, Steven.Goossens@ugent.be.
Department of Diagnostic Sciences, Ghent University, Ghent, Belgium, Steven.Goossens@ugent.be.

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