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Synthetic lethal metabolic targeting of cellular senescence in cancer therapy

Author

Listed:
  • Jan R. Dörr

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany)

  • Yong Yu

    (Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Straße 10, 13125 Berlin, Germany)

  • Maja Milanovic

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany)

  • Gregor Beuster

    (Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Straße 10, 13125 Berlin, Germany)

  • Christin Zasada

    (Integrative Metabolomics and Proteomics, Berlin Institute of Medical Systems Biology, Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Straße 10, 13125 Berlin, Germany)

  • J. Henry M. Däbritz

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany)

  • Jan Lisec

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany
    German Cancer Consortium, Deutsches Krebsforschungzentrum (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany)

  • Dido Lenze

    (Charité-Universitätsmedizin Berlin, Charitéplatz 1, Berlin 10117, Germany)

  • Anne Gerhardt

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany)

  • Katharina Schleicher

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany)

  • Susanne Kratzat

    (Technische Universität München, Ismaninger Straße 22, 81675 Munich, Germany)

  • Bettina Purfürst

    (Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Straße 10, 13125 Berlin, Germany)

  • Stefan Walenta

    (Universitätsmedizin der Johannes Gutenberg-Universität, Institute of Physiology and Pathophysiology, Duesbergweg 6, 55128 Mainz, Germany)

  • Wolfgang Mueller-Klieser

    (Universitätsmedizin der Johannes Gutenberg-Universität, Institute of Physiology and Pathophysiology, Duesbergweg 6, 55128 Mainz, Germany)

  • Markus Gräler

    (Universitätsklinikum Jena, Erlanger Allee 1, 07747 Jena, Germany)

  • Michael Hummel

    (Charité-Universitätsmedizin Berlin, Charitéplatz 1, Berlin 10117, Germany)

  • Ulrich Keller

    (Technische Universität München, Ismaninger Straße 22, 81675 Munich, Germany)

  • Andreas K. Buck

    (Universitätsklinikum Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany)

  • Bernd Dörken

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany
    Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Straße 10, 13125 Berlin, Germany)

  • Lothar Willmitzer

    (Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476 Potsdam, Germany)

  • Maurice Reimann

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany)

  • Stefan Kempa

    (Integrative Metabolomics and Proteomics, Berlin Institute of Medical Systems Biology, Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Straße 10, 13125 Berlin, Germany)

  • Soyoung Lee

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany
    Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Straße 10, 13125 Berlin, Germany)

  • Clemens A. Schmitt

    (Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany
    Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Straße 10, 13125 Berlin, Germany)

Abstract

In mice with Eµ-myc transgenic lymphomas in which therapy-induced senescence (TIS) depends on the H3K9 histone methyltransferase Suv39h1, TIS-competent lymphomas but not TIS-incompetent Suv39h1– lymphomas show increased glucose utilization and ATP production after senescence-inducing chemotherapy to cope with proteotoxic stress elicited by factors of the senescence-associated secretory phenotype (SASP); senescent cancers are selectively vulnerable to drugs that block glucose utilization or autophagy.

Suggested Citation

  • Jan R. Dörr & Yong Yu & Maja Milanovic & Gregor Beuster & Christin Zasada & J. Henry M. Däbritz & Jan Lisec & Dido Lenze & Anne Gerhardt & Katharina Schleicher & Susanne Kratzat & Bettina Purfürst & S, 2013. "Synthetic lethal metabolic targeting of cellular senescence in cancer therapy," Nature, Nature, vol. 501(7467), pages 421-425, September.
    • Handle: RePEc:nat:nature:v:501:y:2013:i:7467:d:10.1038_nature12437
    DOI: 10.1038/nature12437
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    Cited by:

    1. Chen Wang & Hideki Tanizawa & Connor Hill & Aaron Havas & Qiang Zhang & Liping Liao & Xue Hao & Xue Lei & Lu Wang & Hao Nie & Yuan Qi & Bin Tian & Alessandro Gardini & Andrew V. Kossenkov & Aaron Gold, 2024. "METTL3-mediated chromatin contacts promote stress granule phase separation through metabolic reprogramming during senescence," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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