Inactivation of kindlin-3 increases human melanoma aggressiveness through the collagen-activated tyrosine kinase receptor DDR1.


Journal

Oncogene
ISSN: 1476-5594
Titre abrégé: Oncogene
Pays: England
ID NLM: 8711562

Informations de publication

Date de publication:
03 Apr 2024
Historique:
received: 30 05 2023
accepted: 21 03 2024
revised: 15 03 2024
medline: 4 4 2024
pubmed: 4 4 2024
entrez: 3 4 2024
Statut: aheadofprint

Résumé

The role of the focal adhesion protein kindlin-3 as a tumor suppressor and its interaction mechanisms with extracellular matrix constitute a major field of investigation to better decipher tumor progression. Besides the well-described role of kindlin-3 in integrin activation, evidence regarding modulatory functions between melanoma cells and tumor microenvironment are lacking and data are needed to understand mechanisms driven by kindlin-3 inactivation. Here, we show that kindlin-3 inactivation through knockdown or somatic mutations increases BRAF

Identifiants

pubmed: 38570692
doi: 10.1038/s41388-024-03014-3
pii: 10.1038/s41388-024-03014-3
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Coralie Reger De Moura (C)

Department of Pharmacology and Tumor Genomics, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.
Université Paris Cité, INSERM UMR-S 976, Team 1, Human Immunology Pathophysiology & Immunotherapy (HIPI), F-75010, Paris, France.

Baptiste Louveau (B)

Department of Pharmacology and Tumor Genomics, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.
Université Paris Cité, INSERM UMR-S 976, Team 1, Human Immunology Pathophysiology & Immunotherapy (HIPI), F-75010, Paris, France.

Fanélie Jouenne (F)

Department of Pharmacology and Tumor Genomics, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.
Université Paris Cité, INSERM UMR-S 976, Team 1, Human Immunology Pathophysiology & Immunotherapy (HIPI), F-75010, Paris, France.

Paul Vilquin (P)

Department of Pharmacology and Tumor Genomics, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.

Maxime Battistella (M)

Department of Pathology, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.

Yaelle Bellahsen-Harrar (Y)

Department of Pathology, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.

Aurélie Sadoux (A)

Department of Pharmacology and Tumor Genomics, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.

Suzanne Menashi (S)

Department of Pharmacology and Tumor Genomics, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.
Université Paris Cité, INSERM UMR-S 976, Team 1, Human Immunology Pathophysiology & Immunotherapy (HIPI), F-75010, Paris, France.

Nicolas Dumaz (N)

Université Paris Cité, INSERM UMR-S 976, Team 1, Human Immunology Pathophysiology & Immunotherapy (HIPI), F-75010, Paris, France.

Céleste Lebbé (C)

Université Paris Cité, INSERM UMR-S 976, Team 1, Human Immunology Pathophysiology & Immunotherapy (HIPI), F-75010, Paris, France.
Department of Dermatology and CIC, Hôpital Saint Louis, Cancer Institute, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France.

Samia Mourah (S)

Department of Pharmacology and Tumor Genomics, Hôpital Saint Louis, Assistance Publique-Hôpitaux de Paris, F-75010, Paris, France. samia.mourah@aphp.fr.
Université Paris Cité, INSERM UMR-S 976, Team 1, Human Immunology Pathophysiology & Immunotherapy (HIPI), F-75010, Paris, France. samia.mourah@aphp.fr.

Classifications MeSH