Transcription factor NKX2-1 drives serine and glycine synthesis addiction in cancer.


Journal

British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635

Informations de publication

Date de publication:
05 2023
Historique:
received: 16 01 2023
accepted: 21 02 2023
revised: 10 02 2023
medline: 1 5 2023
pubmed: 19 3 2023
entrez: 18 3 2023
Statut: ppublish

Résumé

One-third of cancers activate endogenous synthesis of serine/glycine, and can become addicted to this pathway to sustain proliferation and survival. Mechanisms driving this metabolic rewiring remain largely unknown. NKX2-1 overexpressing and NKX2-1 knockdown/knockout T-cell leukaemia and lung cancer cell line models were established to study metabolic rewiring using ChIP-qPCR, immunoblotting, mass spectrometry, and proliferation and invasion assays. Findings and therapeutic relevance were validated in mouse models and confirmed in patient datasets. Exploring T-cell leukaemia, lung cancer and neuroendocrine prostate cancer patient datasets highlighted the transcription factor NKX2-1 as putative driver of serine/glycine metabolism. We demonstrate that transcription factor NKX2-1 binds and transcriptionally upregulates serine/glycine synthesis enzyme genes, enabling NKX2-1 expressing cells to proliferate and invade in serine/glycine-depleted conditions. NKX2-1 driven serine/glycine synthesis generates nucleotides and redox molecules, and is associated with an altered cellular lipidome and methylome. Accordingly, NKX2-1 tumour-bearing mice display enhanced tumour aggressiveness associated with systemic metabolic rewiring. Therapeutically, NKX2-1-expressing cancer cells are more sensitive to serine/glycine conversion inhibition by repurposed anti-depressant sertraline, and to etoposide chemotherapy. Collectively, we identify NKX2-1 as a novel transcriptional regulator of serine/glycine synthesis addiction across cancers, revealing a therapeutic vulnerability of NKX2-1-driven cancers. Transcription factor NKX2-1 fuels cancer cell proliferation and survival by hyperactivating serine/glycine synthesis, highlighting this pathway as a novel therapeutic target in NKX2-1-positive cancers.

Sections du résumé

BACKGROUND
One-third of cancers activate endogenous synthesis of serine/glycine, and can become addicted to this pathway to sustain proliferation and survival. Mechanisms driving this metabolic rewiring remain largely unknown.
METHODS
NKX2-1 overexpressing and NKX2-1 knockdown/knockout T-cell leukaemia and lung cancer cell line models were established to study metabolic rewiring using ChIP-qPCR, immunoblotting, mass spectrometry, and proliferation and invasion assays. Findings and therapeutic relevance were validated in mouse models and confirmed in patient datasets.
RESULTS
Exploring T-cell leukaemia, lung cancer and neuroendocrine prostate cancer patient datasets highlighted the transcription factor NKX2-1 as putative driver of serine/glycine metabolism. We demonstrate that transcription factor NKX2-1 binds and transcriptionally upregulates serine/glycine synthesis enzyme genes, enabling NKX2-1 expressing cells to proliferate and invade in serine/glycine-depleted conditions. NKX2-1 driven serine/glycine synthesis generates nucleotides and redox molecules, and is associated with an altered cellular lipidome and methylome. Accordingly, NKX2-1 tumour-bearing mice display enhanced tumour aggressiveness associated with systemic metabolic rewiring. Therapeutically, NKX2-1-expressing cancer cells are more sensitive to serine/glycine conversion inhibition by repurposed anti-depressant sertraline, and to etoposide chemotherapy.
CONCLUSION
Collectively, we identify NKX2-1 as a novel transcriptional regulator of serine/glycine synthesis addiction across cancers, revealing a therapeutic vulnerability of NKX2-1-driven cancers. Transcription factor NKX2-1 fuels cancer cell proliferation and survival by hyperactivating serine/glycine synthesis, highlighting this pathway as a novel therapeutic target in NKX2-1-positive cancers.

Identifiants

pubmed: 36932191
doi: 10.1038/s41416-023-02216-y
pii: 10.1038/s41416-023-02216-y
pmc: PMC10147615
doi:

Substances chimiques

Glycine TE7660XO1C
NKX2-1 protein, human 0
Nkx2-1 protein, mouse 0
Serine 452VLY9402
Thyroid Nuclear Factor 1 0
Transcription Factors 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1862-1878

Informations de copyright

© 2023. The Author(s).

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Auteurs

Elien Heylen (E)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium.
Leuven Cancer Institute (LKI), Leuven, Belgium.

Paulien Verstraete (P)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium.
Leuven Cancer Institute (LKI), Leuven, Belgium.

Linde Van Aerschot (L)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium.
Leuven Cancer Institute (LKI), Leuven, Belgium.

Shauni L Geeraerts (SL)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium.
Leuven Cancer Institute (LKI), Leuven, Belgium.

Tom Venken (T)

Laboratory for Translational Genetics, Department of Human Genetics, KU Leuven, Leuven, Belgium.
Center for Cancer Biology, VIB, Leuven, Belgium.

Kalina Timcheva (K)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium.
Leuven Cancer Institute (LKI), Leuven, Belgium.

David Nittner (D)

Histopathology Expertise Center, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Department of Oncology, KU Leuven, Leuven, Belgium.

Jelle Verbeeck (J)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium.
Leuven Cancer Institute (LKI), Leuven, Belgium.

Jonathan Royaert (J)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium.
Leuven Cancer Institute (LKI), Leuven, Belgium.

Marion Gijbels (M)

Department of Pathology, GROW School for Oncology and Reproduction, Maastricht, The Netherlands.
Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Cardiovascular Sciences, Amsterdam Infection and Immunity, Amsterdam UMC, Amsterdam, The Netherlands.

Anne Uyttebroeck (A)

Leuven Cancer Institute (LKI), Leuven, Belgium.
Paediatric Haematology and Oncology, University Hospitals Leuven, Leuven, Belgium.
Department of Oncology, Paediatric Oncology, KU Leuven, Leuven, Belgium.

Heidi Segers (H)

Leuven Cancer Institute (LKI), Leuven, Belgium.
Paediatric Haematology and Oncology, University Hospitals Leuven, Leuven, Belgium.
Department of Oncology, Paediatric Oncology, KU Leuven, Leuven, Belgium.

Diether Lambrechts (D)

Laboratory for Translational Genetics, Department of Human Genetics, KU Leuven, Leuven, Belgium.
Center for Cancer Biology, VIB, Leuven, Belgium.

Jan Cools (J)

Leuven Cancer Institute (LKI), Leuven, Belgium.
Center for Cancer Biology, VIB, Leuven, Belgium.
Laboratory of Molecular Biology of Leukemia, Department of Human Genetics, KU Leuven, Leuven, Belgium.

Kim De Keersmaecker (K)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium. kim.dekeersmaecker@kuleuven.be.
Leuven Cancer Institute (LKI), Leuven, Belgium. kim.dekeersmaecker@kuleuven.be.

Kim R Kampen (KR)

Laboratory for Disease Mechanisms in Cancer, Department of Oncology, KU Leuven, Leuven, Belgium. k.kampen@maastrichtuniversity.nl.
Leuven Cancer Institute (LKI), Leuven, Belgium. k.kampen@maastrichtuniversity.nl.
Maastricht University Medical Centre, Department of Radiation Oncology (MAASTRO), GROW School for Oncology and Reproduction, Maastricht, The Netherlands. k.kampen@maastrichtuniversity.nl.

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