Fat1 deletion promotes hybrid EMT state, tumour stemness and metastasis.

Adaptor Proteins, Signal Transducing / metabolism Animals Cadherins / deficiency Carcinoma, Squamous Cell / genetics Disease Progression Enhancer of Zeste Homolog 2 Protein / metabolism Epithelial Cells / metabolism Epithelial-Mesenchymal Transition / drug effects Gene Deletion Gene Expression Regulation, Neoplastic Humans Hyaluronan Receptors / metabolism Lung Neoplasms / genetics Mesoderm / metabolism Mice Neoplasm Metastasis / drug therapy Neoplasms / drug therapy Neoplastic Stem Cells / metabolism Phenotype Phosphoproteins / analysis Proteomics SOXB1 Transcription Factors / metabolism Signal Transduction Skin Neoplasms / genetics Transcription Factors / metabolism YAP-Signaling Proteins Zinc Finger E-box-Binding Homeobox 1 / metabolism src-Family Kinases / metabolism

Journal

Nature

ISSN: 1476-4687

Titre abrégé: Nature

Pays: England

ID NLM: 0410462

Informations de publication

Date de publication:
01 2021

Historique:

received: 21 01 2019

accepted: 26 10 2020

pubmed: 18 12 2020

medline: 27 2 2021

entrez: 17 12 2020

Statut: ppublish

Résumé

FAT1, which encodes a protocadherin, is one of the most frequently mutated genes in human cancers

Identifiants

DOI: 10.1038/s41586-020-03046-1 PMID: 33328637 PMC: PMC7612440

pubmed: 33328637

doi: 10.1038/s41586-020-03046-1

pii: 10.1038/s41586-020-03046-1

pmc: PMC7612440

mid: EMS142166

doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0

Cadherins 0

Cd44 protein, mouse 0

FAT1 protein, human 0

Hyaluronan Receptors 0

Phosphoproteins 0

SOX2 protein, human 0

SOXB1 Transcription Factors 0

Transcription Factors 0

YAP-Signaling Proteins 0

YAP1 protein, human 0

ZEB1 protein, mouse 0

Zinc Finger E-box-Binding Homeobox 1 0

fat1 protein, mouse 0

Enhancer of Zeste Homolog 2 Protein EC 2.1.1.43

Ezh2 protein, mouse EC 2.1.1.43

src-Family Kinases EC 2.7.10.2

Types de publication

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

Langues

eng

Sous-ensembles de citation

Pagination

448-455

Subventions

Organisme : European Research Council

ID : 885093

Pays : International

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