EFA6B regulates a stop signal for collective invasion in breast cancer.


Journal

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

Informations de publication

Date de publication:
13 04 2021
Historique:
received: 26 12 2019
accepted: 18 03 2021
entrez: 14 4 2021
pubmed: 15 4 2021
medline: 29 4 2021
Statut: epublish

Résumé

Cancer is initiated by somatic mutations in oncogenes or tumor suppressor genes. However, additional alterations provide selective advantages to the tumor cells to resist treatment and develop metastases. Their identification is of paramount importance. Reduced expression of EFA6B (Exchange Factor for ARF6, B) is associated with breast cancer of poor prognosis. Here, we report that loss of EFA6B triggers a transcriptional reprogramming of the cell-to-ECM interaction machinery and unleashes CDC42-dependent collective invasion in collagen. In xenograft experiments, MCF10 DCIS.com cells, a DCIS-to-IDC transition model, invades faster when knocked-out for EFA6B. In addition, invasive and metastatic tumors isolated from patients have lower expression of EFA6B and display gene ontology signatures identical to those of EFA6B knock-out cells. Thus, we reveal an EFA6B-regulated molecular mechanism that controls the invasive potential of mammary cells; this finding opens up avenues for the treatment of invasive breast cancer.

Identifiants

pubmed: 33850160
doi: 10.1038/s41467-021-22522-4
pii: 10.1038/s41467-021-22522-4
pmc: PMC8044243
doi:

Substances chimiques

Guanine Nucleotide Exchange Factors 0
PSD4 protein, human 0
CDC42 protein, human EC 3.6.5.2
cdc42 GTP-Binding Protein EC 3.6.5.2

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2198

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Auteurs

Racha Fayad (R)

CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d'Azur, Valbonne, France.

Monserrat Vázquez Rojas (MV)

CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d'Azur, Valbonne, France.

Mariagrazia Partisani (M)

CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d'Azur, Valbonne, France.

Pascal Finetti (P)

INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105, Marseille, France.

Shiraz Dib (S)

CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d'Azur, Valbonne, France.

Sophie Abelanet (S)

CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d'Azur, Valbonne, France.

Virginie Virolle (V)

CNRS UMR7277, Inserm U1091, Institut de Biologie Valrose, Université Côte D'Azur, Nice, France.

Anne Farina (A)

INSERM U1068, Centre de Recherche en Cancérologie de Marseille, ICEP Platform, Aix-Marseille Université UM105, Marseille, France.

Olivier Cabaud (O)

INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105, Marseille, France.

Marc Lopez (M)

INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105, Marseille, France.

Daniel Birnbaum (D)

INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105, Marseille, France.

François Bertucci (F)

INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105, Marseille, France.

Michel Franco (M)

CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d'Azur, Valbonne, France.

Frédéric Luton (F)

CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d'Azur, Valbonne, France. luton@ipmc.cnrs.fr.

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