Metabolic memory underlying minimal residual disease in breast cancer.


Journal

Molecular systems biology
ISSN: 1744-4292
Titre abrégé: Mol Syst Biol
Pays: England
ID NLM: 101235389

Informations de publication

Date de publication:
10 2021
Historique:
revised: 23 09 2021
received: 24 11 2020
accepted: 29 09 2021
entrez: 25 10 2021
pubmed: 26 10 2021
medline: 27 1 2022
Statut: ppublish

Résumé

Tumor relapse from treatment-resistant cells (minimal residual disease, MRD) underlies most breast cancer-related deaths. Yet, the molecular characteristics defining their malignancy have largely remained elusive. Here, we integrated multi-omics data from a tractable organoid system with a metabolic modeling approach to uncover the metabolic and regulatory idiosyncrasies of the MRD. We find that the resistant cells, despite their non-proliferative phenotype and the absence of oncogenic signaling, feature increased glycolysis and activity of certain urea cycle enzyme reminiscent of the tumor. This metabolic distinctiveness was also evident in a mouse model and in transcriptomic data from patients following neo-adjuvant therapy. We further identified a marked similarity in DNA methylation profiles between tumor and residual cells. Taken together, our data reveal a metabolic and epigenetic memory of the treatment-resistant cells. We further demonstrate that the memorized elevated glycolysis in MRD is crucial for their survival and can be targeted using a small-molecule inhibitor without impacting normal cells. The metabolic aberrances of MRD thus offer new therapeutic opportunities for post-treatment care to prevent breast tumor recurrence.

Identifiants

pubmed: 34694069
doi: 10.15252/msb.202010141
pmc: PMC8543468
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

e10141

Subventions

Organisme : Medical Research Council
ID : MC_UU_00025/11
Pays : United Kingdom

Informations de copyright

© 2021 The Authors. Published under the terms of the CC BY 4.0 license.

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Auteurs

Ksenija Radic Shechter (K)

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.

Eleni Kafkia (E)

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
The Medical Research Council Toxicology Unit, University of Cambridge, Cambridge, UK.

Katharina Zirngibl (K)

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
The Medical Research Council Toxicology Unit, University of Cambridge, Cambridge, UK.

Sylwia Gawrzak (S)

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.

Ashna Alladin (A)

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.

Daniel Machado (D)

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.

Christian Lüchtenborg (C)

Biochemie-Zentrum der Universität Heidelberg (BZH), Heidelberg, Germany.

Daniel C Sévin (DC)

Cellzome GmbH, Functional Genomics, GlaxoSmithKline, Heidelberg, Germany.

Britta Brügger (B)

Biochemie-Zentrum der Universität Heidelberg (BZH), Heidelberg, Germany.

Kiran R Patil (KR)

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
The Medical Research Council Toxicology Unit, University of Cambridge, Cambridge, UK.

Martin Jechlinger (M)

European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
MOLIT Institute gGmbH, Heilbronn, Germany.

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