Impairing hydrolase transport machinery prevents human melanoma metastasis.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
15 May 2024
Historique:
received: 30 05 2023
accepted: 29 04 2024
medline: 16 5 2024
pubmed: 16 5 2024
entrez: 15 5 2024
Statut: epublish

Résumé

Metastases are the major cause of cancer-related death, yet, molecular weaknesses that could be exploited to prevent tumor cells spreading are poorly known. Here, we found that perturbing hydrolase transport to lysosomes by blocking either the expression of IGF2R, the main receptor responsible for their trafficking, or GNPT, a transferase involved in the addition of the specific tag recognized by IGF2R, reduces melanoma invasiveness potential. Mechanistically, we demonstrate that the perturbation of this traffic, leads to a compensatory lysosome neo-biogenesis devoided of degradative enzymes. This regulatory loop relies on the stimulation of TFEB transcription factor expression. Interestingly, the inhibition of this transcription factor playing a key role of lysosome production, restores melanomas' invasive potential in the absence of hydrolase transport. These data implicate that targeting hydrolase transport in melanoma could serve to develop new therapies aiming to prevent metastasis by triggering a physiological response stimulating TFEB expression in melanoma.

Identifiants

pubmed: 38750105
doi: 10.1038/s42003-024-06261-y
pii: 10.1038/s42003-024-06261-y
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

574

Informations de copyright

© 2024. The Author(s).

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Auteurs

Alice Nordlinger (A)

INSERM 1279, Tumor Cell Dynamics, Gustave Roussy, Université Paris-Saclay, Villejuif, France.

Justine Del Rio (J)

INSERM 1279, Tumor Cell Dynamics, Gustave Roussy, Université Paris-Saclay, Villejuif, France.

Shivang Parikh (S)

The Ragon Institute of MGH, MIT, and Harvard University, Cambridge, MA, USA.

Laetitia Thomas (L)

INSERM 1279, Tumor Cell Dynamics, Gustave Roussy, Université Paris-Saclay, Villejuif, France.

Roma Parikh (R)

Institute of Pathology, E. Wolfson Medical Center, Holon, Israel.

Hananya Vaknine (H)

Institute of Pathology, E. Wolfson Medical Center, Holon, Israel.

Ronen Brenner (R)

Institute of Pathology, E. Wolfson Medical Center, Holon, Israel.

Francesco Baschieri (F)

INSERM 1279, Tumor Cell Dynamics, Gustave Roussy, Université Paris-Saclay, Villejuif, France.
Institute of Pathophysiology, Innsbruck, Austria.

Aude Robert (A)

INSERM 1279, Tumor Cell Dynamics, Gustave Roussy, Université Paris-Saclay, Villejuif, France.

Mehdi Khaled (M)

INSERM 1279, Tumor Cell Dynamics, Gustave Roussy, Université Paris-Saclay, Villejuif, France. mehdi.khaled@gustaveroussy.fr.

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