Synthetic lethal metabolic targeting of cellular senescence in cancer therapy

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, Stefan Walenta, Wolfgang Mueller-Klieser, Markus Gräler, Michael Hummel, Ulrich Keller, Andreas K. Buck, Bernd Dörken, Lothar Willmitzer, Maurice Reimann, Stefan Kempa, Soyoung Lee and Clemens A. Schmitt ()
Additional contact information
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
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
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
Clemens A. Schmitt: Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany

Nature, 2013, vol. 501, issue 7467, 421-425

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.

Date: 2013
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DOI: 10.1038/nature12437

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