A thiol-bound drug reservoir enhances APR-246-induced mutant p53 tumor cell death.


Journal

EMBO molecular medicine
ISSN: 1757-4684
Titre abrégé: EMBO Mol Med
Pays: England
ID NLM: 101487380

Informations de publication

Date de publication:
05 02 2021
Historique:
received: 07 05 2019
revised: 16 11 2020
accepted: 17 11 2020
pubmed: 15 12 2020
medline: 25 11 2021
entrez: 14 12 2020
Statut: ppublish

Résumé

The tumor suppressor gene TP53 is the most frequently mutated gene in cancer. The compound APR-246 (PRIMA-1Met/Eprenetapopt) is converted to methylene quinuclidinone (MQ) that targets mutant p53 protein and perturbs cellular antioxidant balance. APR-246 is currently tested in a phase III clinical trial in myelodysplastic syndrome (MDS). By in vitro, ex vivo, and in vivo models, we show that combined treatment with APR-246 and inhibitors of efflux pump MRP1/ABCC1 results in synergistic tumor cell death, which is more pronounced in TP53 mutant cells. This is associated with altered cellular thiol status and increased intracellular glutathione-conjugated MQ (GS-MQ). Due to the reversibility of MQ conjugation, GS-MQ forms an intracellular drug reservoir that increases availability of MQ for targeting mutant p53. Our study shows that redox homeostasis is a critical determinant of the response to mutant p53-targeted cancer therapy.

Identifiants

pubmed: 33314700
doi: 10.15252/emmm.201910852
pmc: PMC7863383
doi:

Substances chimiques

Pharmaceutical Preparations 0
Quinuclidines 0
Sulfhydryl Compounds 0
Tumor Suppressor Protein p53 0
eprenetapopt Z41TGB4080

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

e10852

Subventions

Organisme : Medical Research Council
ID : RG84369
Pays : United Kingdom
Organisme : Cancer Research UK
ID : RG81771/84119
Pays : United Kingdom

Informations de copyright

© 2020 The Authors. Published under the terms of the CC BY 4.0 license.

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Auteurs

Sophia Ceder (S)

Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.

Sofi E Eriksson (SE)

Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.

Emarndeena H Cheteh (EH)

Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.

Swati Dawar (S)

Peter MacCallum Cancer Centre, Melbourne, Vic., Australia.

Mariana Corrales Benitez (M)

Peter MacCallum Cancer Centre, Melbourne, Vic., Australia.

Vladimir J N Bykov (VJN)

Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.

Kenji M Fujihara (KM)

Peter MacCallum Cancer Centre, Melbourne, Vic., Australia.
Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Vic., Australia.

Mélodie Grandin (M)

Department of Clinical Pathology, The University of Melbourne, Melbourne, Vic., Australia.
Victorian Comprehensive Cancer Centre, University of Melbourne Centre for Cancer Research, Melbourne, Vic., Australia.

Xiaodun Li (X)

MRC Cancer Unit, University of Cambridge, Cambridge, UK.

Susanne Ramm (S)

Peter MacCallum Cancer Centre, Victorian Centre for Functional Genomics, Melbourne, Vic., Australia.

Corina Behrenbruch (C)

Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Vic., Australia.
Department of Clinical Pathology, The University of Melbourne, Melbourne, Vic., Australia.

Kaylene J Simpson (KJ)

Peter MacCallum Cancer Centre, Victorian Centre for Functional Genomics, Melbourne, Vic., Australia.

Frédéric Hollande (F)

Department of Clinical Pathology, The University of Melbourne, Melbourne, Vic., Australia.
Victorian Comprehensive Cancer Centre, University of Melbourne Centre for Cancer Research, Melbourne, Vic., Australia.

Lars Abrahmsen (L)

Aprea Therapeutics AB, Solna, Sweden.

Nicholas J Clemons (NJ)

Peter MacCallum Cancer Centre, Melbourne, Vic., Australia.
Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Vic., Australia.

Klas G Wiman (KG)

Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.

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