Pharmacological targeting of netrin-1 inhibits EMT in cancer.
Animals
Humans
Mice
A549 Cells
Carcinoma, Squamous Cell
/ drug therapy
Cell Line, Tumor
Epithelial-Mesenchymal Transition
/ drug effects
Netrin Receptors
/ antagonists & inhibitors
Netrin-1
/ antagonists & inhibitors
RNA, Small Interfering
/ genetics
Disease Models, Animal
Skin Neoplasms
/ drug therapy
Antibodies, Monoclonal
/ pharmacology
Neoplasm Metastasis
/ drug therapy
Single-Cell Gene Expression Analysis
RNA-Seq
Epithelial Cell Adhesion Molecule
/ metabolism
Xenograft Model Antitumor Assays
Transforming Growth Factor beta1
/ pharmacology
Journal
Nature
ISSN: 1476-4687
Titre abrégé: Nature
Pays: England
ID NLM: 0410462
Informations de publication
Date de publication:
Aug 2023
Aug 2023
Historique:
received:
04
04
2022
accepted:
26
06
2023
pmc-release:
01
02
2024
medline:
11
8
2023
pubmed:
3
8
2023
entrez:
2
8
2023
Statut:
ppublish
Résumé
Epithelial-to-mesenchymal transition (EMT) regulates tumour initiation, progression, metastasis and resistance to anti-cancer therapy
Identifiants
pubmed: 37532929
doi: 10.1038/s41586-023-06372-2
pii: 10.1038/s41586-023-06372-2
pmc: PMC7615210
mid: EMS188994
doi:
Substances chimiques
Netrin Receptors
0
Netrin-1
158651-98-0
RNA, Small Interfering
0
Antibodies, Monoclonal
0
Unc5b protein, mouse
0
Epithelial Cell Adhesion Molecule
0
TGFB1 protein, human
0
Transforming Growth Factor beta1
0
Ntn1 protein, mouse
0
NTN1 protein, human
0
Banques de données
ClinicalTrials.gov
['NCT02977195']
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
402-408Subventions
Organisme : European Research Council
ID : 885093
Pays : International
Informations de copyright
© 2023. The Author(s), under exclusive licence to Springer Nature Limited.
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