Synthetic lethal metabolic targeting of cellular senescence in cancer therapy (original) (raw)
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Accessions
Gene Expression Omnibus
Data deposits
Microarray data are deposited at the Gene Expression Omnibus under accession numbers GSE31099 and GSE44355.
Change history
20 August 2013
Source Data files for Figs 1–4 were added.
References
- Narita, M. et al. Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence. Cell 113, 703–716 (2003)
CAS PubMed Google Scholar - Braig, M. et al. Oncogene-induced senescence as an initial barrier in lymphoma development. Nature 436, 660–665 (2005)
CAS PubMed ADS Google Scholar - Schmitt, C. A. et al. A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy. Cell 109, 335–346 (2002)
CAS PubMed Google Scholar - Acosta, J. C. et al. Chemokine signaling via the CXCR2 receptor reinforces senescence. Cell 133, 1006–1018 (2008)
CAS PubMed Google Scholar - Coppe, J. P. et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol. 6, e301 (2008)
PubMed Central Google Scholar - Kuilman, T. et al. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell 133, 1019–1031 (2008)
CAS PubMed Google Scholar - Campisi, J. & d'Adda di Fagagna, F. Cellular senescence: when bad things happen to good cells. Nature Rev. Mol. Cell Biol. 8, 729–740 (2007)
CAS Google Scholar - Collado, M. & Serrano, M. Senescence in tumours: evidence from mice and humans. Nature Rev. Cancer 10, 51–57 (2010)
CAS Google Scholar - Kuilman, T., Michaloglou, C., Mooi, W. J. & Peeper, D. S. The essence of senescence. Genes Dev. 24, 2463–2479 (2010)
CAS PubMed PubMed Central Google Scholar - Nardella, C., Clohessy, J. G., Alimonti, A. & Pandolfi, P. P. Pro-senescence therapy for cancer treatment. Nature Rev. Cancer 11, 503–511 (2011)
CAS Google Scholar - Dimri, G. P. et al. A biomarker that identifies senescent human cells in culture and in aging skin in vivo. Proc. Natl Acad. Sci. USA 92, 9363–9367 (1995)
CAS ADS PubMed PubMed Central Google Scholar - Moskowitz, C. H. et al. Risk-adapted dose-dense immunochemotherapy determined by interim FDG-PET in advanced-stage diffuse large B-cell lymphoma. J. Clin. Oncol. 28, 1896–1903 (2010)
CAS PubMed PubMed Central Google Scholar - Jones, R. G. et al. AMP-activated protein kinase induces a p53-dependent metabolic checkpoint. Mol. Cell 18, 283–293 (2005)
CAS PubMed Google Scholar - Warburg, O., Posener, K. & Negelein, E. Über den Stoffwechsel der Carcinomzelle. Biochem. Z. 152, 319–344 (1924)
Google Scholar - Vander Heiden, M. G. et al. Evidence for an alternative glycolytic pathway in rapidly proliferating cells. Science 329, 1492–1499 (2010)
CAS PubMed ADS Google Scholar - Young, A. R. et al. Autophagy mediates the mitotic senescence transition. Genes Dev. 23, 798–803 (2009)
CAS PubMed PubMed Central Google Scholar - Chien, Y. et al. Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity. Genes Dev. 25, 2125–2136 (2011)
CAS PubMed PubMed Central Google Scholar - Jing, H. et al. Opposing roles of NF-κB in anti-cancer treatment outcome unveiled by cross-species investigations. Genes Dev. 25, 2137–2146 (2011)
CAS PubMed PubMed Central Google Scholar - Kroemer, G., Marino, G. & Levine, B. Autophagy and the integrated stress response. Mol. Cell 40, 280–293 (2010)
CAS PubMed PubMed Central Google Scholar - Pankiv, S. et al. p62/SQSTM1 binds directly to Atg8/lymphoma cells3 to facilitate degradation of ubiquitinated protein aggregates by autophagy. J. Biol. Chem. 282, 24131–24145 (2007)
CAS PubMed Google Scholar - Nakagawa, T. et al. Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta. Nature 403, 98–103 (2000)
CAS PubMed ADS Google Scholar - Kaelin, W. G., Jr The concept of synthetic lethality in the context of anticancer therapy. Nature Rev. Cancer 5, 689–698 (2005)
CAS Google Scholar - Xue, W. et al. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature 445, 656–660 (2007)
CAS PubMed PubMed Central Google Scholar - Kang, T. W. et al. Senescence surveillance of pre-malignant hepatocytes limits liver cancer development. Nature 479, 547–551 (2011)
CAS ADS PubMed Google Scholar - Reimann, M. et al. Tumor stroma-derived TGF-β limits Myc-driven lymphomagenesis via Suv39h1-dependent senescence. Cancer Cell 17, 262–272 (2010)
CAS PubMed Google Scholar - Adams, J. M. et al. The c-myc oncogene driven by immunoglobulin enhancers induces lymphoid malignancy in transgenic mice. Nature 318, 533–538 (1985)
CAS PubMed ADS Google Scholar - Peters, A. H. et al. Loss of the Suv39h histone methyltransferases impairs mammalian heterochromatin and genome stability. Cell 107, 323–337 (2001)
CAS PubMed Google Scholar - Schmitt, C. A. et al. Dissecting p53 tumor suppressor functions in vivo. Cancer Cell 1, 289–298 (2002)
CAS PubMed Google Scholar - Schmitt, C. A., McCurrach, M. E., de Stanchina, E., Wallace-Brodeur, R. R. & Lowe, S. W. INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53. Genes Dev. 13, 2670–2677 (1999)
CAS PubMed PubMed Central Google Scholar - Shields, A. F. et al. Imaging proliferation in vivo with [F-18]FLT and positron emission tomography. Nature Med. 4, 1334–1336 (1998)
CAS PubMed Google Scholar - Marciniak, S. J. et al. CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum. Genes Dev. 18, 3066–3077 (2004)
CAS PubMed PubMed Central Google Scholar - Reimann, M. et al. The Myc-evoked DNA damage response accounts for treatment resistance in primary lymphomas in vivo. Blood 110, 2996–3004 (2007)
CAS PubMed Google Scholar - Subramanian, A. et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc. Natl Acad. Sci. USA 102, 15545–15550 (2005)
CAS ADS PubMed PubMed Central Google Scholar - Walenta, S. et al. High lactate levels predict likelihood of metastases, tumor recurrence, and restricted patient survival in human cervical cancers. Cancer Res. 60, 916–921 (2000)
CAS PubMed Google Scholar - Liu, L. et al. Deregulated MYC expression induces dependence upon AMPK-related kinase 5. Nature 483, 608–612 (2012)
CAS PubMed ADS Google Scholar - Kempa, S. et al. An automated GCxGC-TOF-MS protocol for batch-wise extraction and alignment of mass isotopomer matrixes from differential 13C-labelling experiments: a case study for photoautotrophic-mixotrophic grown Chlamydomonas reinhardtii cells. J. Basic Microbiol. 49, 82–91 (2009)
CAS PubMed Google Scholar - Giavalisco, P. et al. High-resolution direct infusion-based mass spectrometry in combination with whole 13C metabolome isotope labeling allows unambiguous assignment of chemical sum formulas. Anal. Chem. 80, 9417–9425 (2008)
CAS PubMed Google Scholar - Lisec, J., Schauer, N., Kopka, J., Willmitzer, L. & Fernie, A. R. Gas chromatography mass spectrometry-based metabolite profiling in plants. Nature Protocols 1, 387–396 (2006)
CAS PubMed Google Scholar - Cuadros-Inostroza, A. et al. TargetSearch—a Bioconductor package for the efficient preprocessing of GC-MS metabolite profiling data. BMC Bioinformatics 10, 428 (2009)
PubMed PubMed Central Google Scholar - Lisec, J. et al. Corn hybrids display lower metabolite variability and complex metabolite inheritance patterns. Plant J. 68, 326–336 (2011)
CAS PubMed Google Scholar - Stacklies, W., Redestig, H., Scholz, M., Walther, D. & Selbig, J. pcaMethods—a bioconductor package providing PCA methods for incomplete data. Bioinformatics 23, 1164–1167 (2007)
Article CAS PubMed Google Scholar - Bode, C. & Graler, M. H. Quantification of sphingosine-1-phosphate and related sphingolipids by liquid chromatography coupled to tandem mass spectrometry. Methods Mol. Biol. 874, 33–44 (2012)
CAS PubMed Google Scholar - Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D. & Lowe, S. W. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a. Cell 88, 593–602 (1997)
CAS PubMed Google Scholar - Berns, K. et al. A large-scale RNAi screen in human cells identifies new components of the p53 pathway. Nature 428, 431–437 (2004)
CAS PubMed ADS Google Scholar - Reimer, T. A. et al. Reevaluation of the 22-1-1 antibody and its putative antigen, EBAG9/RCAS1, as a tumor marker. BMC Cancer 17, 47 (2005)
Google Scholar - Castro, F. et al. High-throughput SNP-based authentication of human cell lines. Int. J. Cancer 132, 308–314 (2013)
CAS PubMed Google Scholar
Acknowledgements
We thank the late A. Harris, T. Jacks, T. Jenuwein, P. A. Khavari, N. Mizushima, D. Peeper, and M. Vander Heiden for mice, cells and materials; the flow cytometry facility at the Berlin-Brandenburg Center for Regenerative Therapies; N. Burbach, J. Dräger, A. Herrmann, K. Kirste, S. Maßwig, B. Teichmann and S. Spiesicke-Wegener for technical assistance; and members of the Schmitt laboratory for discussions and editorial advice. This work was supported by a Ph.D. fellowship to J.R.D. from the Boehringer Ingelheim Foundation, and grants from the Deutsche Forschungsgemeinschaft to W.M.-K. (MK576/15-1), to U.K. and A.K.B. (SFB 824), to U.K., B.D., S.L. and C.A.S. (SFB/TRR 54), and to C.A.S. from the Helmholtz Association (Helmholtz Alliance ‘Preclinical Comprehensive Cancer Center’; grant no. HA-305) and the Deutsche Krebshilfe (grant no. 108789). This interdisciplinary work was made possible by the structural framework of the inter-institutional cooperation between Charité and MDC (now represented by the Berlin Institute of Health (BIH)), the Berlin School of Integrative Oncology (BSIO) graduate program funded within the Excellence Initiative, and the German Cancer Consortium (GCC).
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Authors and Affiliations
- Charité-Universitätsmedizin Berlin, Molekulares Krebsforschungszentrum (MKFZ), Augustenburger Platz 1, 13353 Berlin, Germany,
Jan R. Dörr, Maja Milanovic, J. Henry M. Däbritz, Jan Lisec, Anne Gerhardt, Katharina Schleicher, Bernd Dörken, Maurice Reimann, Soyoung Lee & Clemens A. Schmitt - Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Straße 10, 13125 Berlin, Germany,
Yong Yu, Gregor Beuster, Bettina Purfürst, Bernd Dörken, Soyoung Lee & Clemens A. Schmitt - Integrative Metabolomics and Proteomics, Berlin Institute of Medical Systems Biology, Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Straße 10, 13125 Berlin, Germany,
Christin Zasada & Stefan Kempa - German Cancer Consortium, Deutsches Krebsforschungzentrum (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany,
Jan Lisec - Department of Pathology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, Berlin 10117, Germany,
Dido Lenze & Michael Hummel - III Medical Department, Technische Universität München, Ismaninger Straße 22, 81675 Munich, Germany,
Susanne Kratzat & Ulrich Keller - Universitätsmedizin der Johannes Gutenberg-Universität, Institute of Physiology and Pathophysiology, Duesbergweg 6, 55128 Mainz, Germany,
Stefan Walenta & Wolfgang Mueller-Klieser - Department of Anesthesiology and Intensive Care Medicine & Center for Sepsis Control and Care (CSCC), Universitätsklinikum Jena, Erlanger Allee 1, 07747 Jena, Germany,
Markus Gräler - Department of Nuclear Medicine, Universitätsklinikum Würzburg, Oberdürrbacher Straße 6, 97080 Würzburg, Germany,
Andreas K. Buck - Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476 Potsdam, Germany,
Lothar Willmitzer
Authors
- 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
- Clemens A. Schmitt
Contributions
J.R.D., S.L. and C.A.S. conceived the project, designed the experiments, and analysed the data, and W.M.-K., U.K., B.D., L.W. and St.K. provided critical input. Y.Y., G.B., C.Z., J.H.M.D., J.L., A.G., K.S., Su.K., S.W., M.G. and M.R. conducted experiments, M.M. compiled GSEA data, D.L. generated gene expression profiling data, M.H. analysed GEP data, B.P. carried out electron microscopy, and A.K.B. performed PET imaging. C.A.S., with editorial assistance from S.L., wrote the manuscript. All authors discussed the results and commented on the manuscript.
Corresponding author
Correspondence toClemens A. Schmitt.
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The authors declare no competing financial interests.
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Dörr, J., Yu, Y., Milanovic, M. et al. Synthetic lethal metabolic targeting of cellular senescence in cancer therapy.Nature 501, 421–425 (2013). https://doi.org/10.1038/nature12437
- Received: 15 November 2011
- Accepted: 04 July 2013
- Published: 14 August 2013
- Issue date: 19 September 2013
- DOI: https://doi.org/10.1038/nature12437