Nuclear-capture of endosomes depletes nuclear G-actin to promote SRF/MRTF activation and cancer cell invasion.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
24 11 2021
Historique:
received: 29 07 2020
accepted: 21 10 2021
entrez: 25 11 2021
pubmed: 26 11 2021
medline: 24 12 2021
Statut: epublish

Résumé

Signals are relayed from receptor tyrosine kinases (RTKs) at the cell surface to effector systems in the cytoplasm and nucleus, and coordination of this process is important for the execution of migratory phenotypes, such as cell scattering and invasion. The endosomal system influences how RTK signalling is coded, but the ways in which it transmits these signals to the nucleus to influence gene expression are not yet clear. Here we show that hepatocyte growth factor, an activator of MET (an RTK), promotes Rab17- and clathrin-dependent endocytosis of EphA2, another RTK, followed by centripetal transport of EphA2-positive endosomes. EphA2 then mediates physical capture of endosomes on the outer surface of the nucleus; a process involving interaction between the nuclear import machinery and a nuclear localisation sequence in EphA2's cytodomain. Nuclear capture of EphA2 promotes RhoG-dependent phosphorylation of the actin-binding protein, cofilin to oppose nuclear import of G-actin. The resulting depletion of nuclear G-actin drives transcription of Myocardin-related transcription factor (MRTF)/serum-response factor (SRF)-target genes to implement cell scattering and the invasive behaviour of cancer cells.

Identifiants

pubmed: 34819513
doi: 10.1038/s41467-021-26839-y
pii: 10.1038/s41467-021-26839-y
pmc: PMC8613289
doi:

Substances chimiques

Actins 0
Ternary Complex Factors 0
Hepatocyte Growth Factor 67256-21-7
Receptor Protein-Tyrosine Kinases EC 2.7.10.1

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

6829

Subventions

Organisme : Cancer Research UK
ID : A18277
Pays : United Kingdom
Organisme : Cancer Research UK
ID : A29800
Pays : United Kingdom
Organisme : Cancer Research UK
ID : A31287
Pays : United Kingdom
Organisme : Cancer Research UK
ID : A17196
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/P01058X/1
Pays : United Kingdom

Informations de copyright

© 2021. The Author(s).

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Auteurs

Sergi Marco (S)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.

Matthew Neilson (M)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.

Madeleine Moore (M)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.

Arantxa Perez-Garcia (A)

Institute of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, Scotland, UK.

Holly Hall (H)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.

Louise Mitchell (L)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.

Sergio Lilla (S)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.

Giovani R Blanco (GR)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.

Ann Hedley (A)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.

Sara Zanivan (S)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK.
Institute of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, Scotland, UK.

Jim C Norman (JC)

CRUK Beatson Institute, Glasgow, G61 1BD, Scotland, UK. j.norman@beatson.gla.ac.uk.
Institute of Cancer Sciences, University of Glasgow, Glasgow, G61 1QH, Scotland, UK. j.norman@beatson.gla.ac.uk.

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