Enhancing chemotherapy response through augmented synthetic lethality by co-targeting nucleotide excision repair and cell-cycle checkpoints.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
17 08 2020
Historique:
received: 16 10 2018
accepted: 22 07 2020
entrez: 19 8 2020
pubmed: 19 8 2020
medline: 9 9 2020
Statut: epublish

Résumé

In response to DNA damage, a synthetic lethal relationship exists between the cell cycle checkpoint kinase MK2 and the tumor suppressor p53. Here, we describe the concept of augmented synthetic lethality (ASL): depletion of a third gene product enhances a pre-existing synthetic lethal combination. We show that loss of the DNA repair protein XPA markedly augments the synthetic lethality between MK2 and p53, enhancing anti-tumor responses alone and in combination with cisplatin chemotherapy. Delivery of siRNA-peptide nanoplexes co-targeting MK2 and XPA to pre-existing p53-deficient tumors in a highly aggressive, immunocompetent mouse model of lung adenocarcinoma improves long-term survival and cisplatin response beyond those of the synthetic lethal p53 mutant/MK2 combination alone. These findings establish a mechanism for co-targeting DNA damage-induced cell cycle checkpoints in combination with repair of cisplatin-DNA lesions in vivo using RNAi nanocarriers, and motivate further exploration of ASL as a generalized strategy to improve cancer treatment.

Identifiants

pubmed: 32807787
doi: 10.1038/s41467-020-17958-z
pii: 10.1038/s41467-020-17958-z
pmc: PMC7431578
doi:

Substances chimiques

RNA, Small Interfering 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

4124

Subventions

Organisme : NCI NIH HHS
ID : R01 CA245314
Pays : United States
Organisme : NIA NIH HHS
ID : K99 AG045144
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA014051
Pays : United States
Organisme : NIBIB NIH HHS
ID : F32 EB017614
Pays : United States
Organisme : NIEHS NIH HHS
ID : R35 ES028374
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM104047
Pays : United States
Organisme : NIA NIH HHS
ID : R00 AG045144
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA226898
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES015339
Pays : United States
Organisme : NCI NIH HHS
ID : R37 CA034992
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA034992
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA211184
Pays : United States

Références

Fleuren, E. D., Zhang, L., Wu, J. & Daly, R. J. The kinome ‘at large’ in cancer. Nat. Rev. Cancer 16, 83–98 (2016).
pubmed: 26822576
Socinski, M. A. Clinical issues in the management of non-small-cell lung cancer and the role of platinum-based therapy. Clin. Lung Cancer 5, 274–289 (2004).
pubmed: 15086966
Ciccia, A. & Elledge, S. J. The DNA damage response: making it safe to play with knives. Mol. Cell 40, 179–204 (2010).
pubmed: 20965415 pmcid: 2988877
Goldstein M., Kastan M. B. The DNA damage response: implications for tumor responses to radiation and chemotherapy. Annu. Rev. Med. 66, 129–143 (2015).
pubmed: 25423595
Wang, D. & Lippard, S. J. Cellular processing of platinum anticancer drugs. Nat. Rev. Drug Discov. 4, 307–320 (2005).
pubmed: 15789122
Jamieson, E. R. & Lippard, S. J. Structure, recognition, and processing of cisplatin-DNA adducts. Chem. Rev. 99, 2467–2498 (1999).
pubmed: 11749487
Galluzzi, L., Vitale, I., Vacchelli, E. & Kroemer, G. Cell death signaling and anticancer therapy. Front Oncol. 1, 5 (2011).
pubmed: 22655227 pmcid: 3356092
Barry, M. A., Behnke, C. A. & Eastman, A. Activation of programmed cell death (apoptosis) by cisplatin, other anticancer drugs, toxins and hyperthermia. Biochem. Pharm. 40, 2353–2362 (1990).
pubmed: 2244936
Bouwman, P. & Jonkers, J. The effects of deregulated DNA damage signalling on cancer chemotherapy response and resistance. Nat. Rev. Cancer 12, 587–598 (2012).
pubmed: 22918414
Oza, A. M. et al. Olaparib combined with chemotherapy for recurrent platinum-sensitive ovarian cancer: a randomised phase 2 trial. Lancet Oncol. 16, 87–97 (2015).
pubmed: 25481791
Cerami, E. et al. The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data. Cancer Discov. 2, 401–404 (2012).
pubmed: 22588877 pmcid: 22588877
Gao, J. et al. Integrative analysis of complex cancer genomics and clinical profiles using the cBioPortal. Sci. Signal. 6, pl1 (2013).
pubmed: 4160307 pmcid: 4160307
Zehir, A. et al. Erratum: Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients. Nat. Med. 23, 1004 (2017).
pubmed: 28777785
Reinhardt, H. C., Aslanian, A. S., Lees, J. A. & Yaffe, M. B. p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. Cancer Cell 11, 175–189 (2007).
pubmed: 17292828 pmcid: 2742175
Cannell, I. G. et al. p38 MAPK/MK2-mediated induction of miR-34c following DNA damage prevents Myc-dependent DNA replication. Proc. Natl Acad. Sci. USA 107, 5375–5380 (2010).
pubmed: 20212154
Reinhardt, H. C. et al. DNA damage activates a spatially distinct late cytoplasmic cell-cycle checkpoint network controlled by MK2-mediated RNA stabilization. Mol. Cell 40, 34–49 (2010).
pubmed: 20932473 pmcid: 3030122
Morandell, S. et al. A reversible gene-targeting strategy identifies synthetic lethal interactions between MK2 and p53 in the DNA damage response in vivo. Cell Rep. 5, 868–877 (2013).
pubmed: 24239348 pmcid: 3962842
Cannell, I. G. et al. A pleiotropic RNA-binding protein controls distinct cell cycle checkpoints to drive resistance of p53-defective tumors to chemotherapy. Cancer Cell 28, 623–637 (2015).
pubmed: 26602816 pmcid: 4830093
Muller, P. A. & Vousden, K. H. p53 mutations in cancer. Nat. Cell Biol. 15, 2–8 (2013).
pubmed: 23263379
Kelland, L. The resurgence of platinum-based cancer chemotherapy. Nat. Rev. Cancer 7, 573–584 (2007).
pubmed: 17625587
Bowden, N. A. Nucleotide excision repair: why is it not used to predict response to platinum-based chemotherapy? Cancer Lett. 346, 163–171 (2014).
pubmed: 24462818
Koberle, B., Masters, J. R., Hartley, J. A. & Wood, R. D. Defective repair of cisplatin-induced DNA damage caused by reduced XPA protein in testicular germ cell tumours. Curr. Biol. 9, 273–276 (1999).
pubmed: 10074455
Welsh, C. et al. Reduced levels of XPA, ERCC1 and XPF DNA repair proteins in testis tumor cell lines. Int J. Cancer 110, 352–361 (2004).
pubmed: 15095299
Shuck, S. C., Short, E. A. & Turchi, J. J. Eukaryotic nucleotide excision repair: from understanding mechanisms to influencing biology. Cell Res. 18, 64–72 (2008).
pubmed: 18166981 pmcid: 2432112
Sirohi, B. et al. Early response to platinum-based first-line chemotherapy in non-small cell lung cancer may predict survival. J. Thorac. Oncol. 2, 735–740 (2007).
pubmed: 17762340
Deans, A. J. & West, S. C. DNA interstrand crosslink repair and cancer. Nat. Rev. Cancer 11, 467–480 (2011).
pubmed: 21701511 pmcid: 3560328
Andreassen, P. R. & Ren, K. Fanconi anemia proteins, DNA interstrand crosslink repair pathways, and cancer therapy. Curr. Cancer Drug Targets 9, 101–117 (2009).
pubmed: 19200054 pmcid: 4934657
Wood, R. D. Mammalian nucleotide excision repair proteins and interstrand crosslink repair. Environ. Mol. Mutagen 51, 520–526 (2010).
pubmed: 20658645 pmcid: 3017513
Scheibye-Knudsen, M., Croteau, D. L. & Bohr, V. A. Mitochondrial deficiency in Cockayne syndrome. Mech. Ageing Dev. 134, 275–283 (2013).
pubmed: 23435289 pmcid: 3663877
Niedernhofer, L. J., Bohr, V. A., Sander, M. & Kraemer, K. H. Xeroderma pigmentosum and other diseases of human premature aging and DNA repair: molecules to patients. Mech. Ageing Dev. 132, 340–347 (2011).
pubmed: 21708183 pmcid: 3474983
Doles, J. et al. Suppression of Rev3, the catalytic subunit of Pol{zeta}, sensitizes drug-resistant lung tumors to chemotherapy. Proc. Natl Acad. Sci. USA 107, 20786–20791 (2010).
pubmed: 21068376
DuPage, M., Dooley, A. L. & Jacks, T. Conditional mouse lung cancer models using adenoviral or lentiviral delivery of Cre recombinase. Nat. Protoc. 4, 1064–1072 (2009).
pubmed: 19561589 pmcid: 2757265
Bartkova, J. et al. DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis. Nature 434, 864–870 (2005).
pubmed: 15829956
Macheret, M. & Halazonetis, T. D. DNA replication stress as a hallmark of cancer. Annu Rev. Pathol. 10, 425–448 (2015).
pubmed: 25621662
Mourey, R. J. et al. A benzothiophene inhibitor of mitogen-activated protein kinase-activated protein kinase 2 inhibits tumor necrosis factor alpha production and has oral anti-inflammatory efficacy in acute and chronic models of inflammation. J. Pharm. Exp. Ther. 333, 797–807 (2010).
Ronkina, N., Kotlyarov, A. & Gaestel, M. MK2 and MK3–a pair of isoenzymes? Front Biosci. 13, 5511–5521 (2008).
pubmed: 18508601
Gaestel, M. MAPKAP kinases—MKs—two’s company, three’s a crowd. Nat. Rev. Mol. Cell Biol. 7, 120–130 (2006).
pubmed: 16421520
Dreaden, E. C. et al. RNA-Peptide nanoplexes drug DNA damage pathways in high-grade serous ovarian tumors. Bioeng. Transl. Med. 3, 26–36 (2018).
pubmed: 29376131 pmcid: 5773954
Nyland, J. F., Bai, J. J., Katz, H. E. & Silbergeld, E. K. In vitro interactions between splenocytes and dansylamide dye-embedded nanoparticles detected by flow cytometry. Nanomedicine 5, 298–304 (2009).
pubmed: 19523425 pmcid: 2735588
Jackson, E. L. et al. The differential effects of mutant p53 alleles on advanced murine lung cancer. Cancer Res. 65, 10280–10288 (2005).
pubmed: 16288016
Sweet-Cordero, A. et al. An oncogenic KRAS2 expression signature identified by cross-species gene-expression analysis. Nat. Genet. 37, 48–55 (2005).
pubmed: 15608639
Jandial, D. D., Messer, K., Farshchi-Heydari, S., Pu, M. & Howell, S. B. Tumor platinum concentration following intraperitoneal administration of cisplatin versus carboplatin in an ovarian cancer model. Gynecol. Oncol. 115, 362–366 (2009).
pubmed: 19775736 pmcid: 3571663
Minchinton, A. I. & Tannock, I. F. Drug penetration in solid tumours. Nat. Rev. Cancer 6, 583–592 (2006).
pubmed: 16862189
Wilhelm S., et al. Analysis of nanoparticle delivery to tumours. Nat. Rev. Mater. 1, 16014 (2016).
Reinhardt, H. C. & Yaffe, M. B. Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2. Curr. Opin. Cell Biol. 21, 245–255 (2009).
pubmed: 2699687 pmcid: 2699687
Sausville, E. et al. Phase I dose-escalation study of AZD7762, a checkpoint kinase inhibitor, in combination with gemcitabine in US patients with advanced solid tumors. Cancer Chemother. Pharm. 73, 539–549 (2014).
Lam, M. H., Liu, Q., Elledge, S. J. & Rosen, J. M. Chk1 is haploinsufficient for multiple functions critical to tumor suppression. Cancer Cell 6, 45–59 (2004).
pubmed: 15261141
Manke, I. A. et al. MAPKAP kinase-2 is a cell cycle checkpoint kinase that regulates the G2/M transition and S phase progression in response to UV irradiation. Mol. Cell 17, 37–48 (2005).
pubmed: 15629715
Coate, L. E., John, T., Tsao, M. S. & Shepherd, F. A. Molecular predictive and prognostic markers in non-small-cell lung cancer. Lancet Oncol. 10, 1001–1010 (2009).
pubmed: 19796752
Spitz, M. R., Wei, Q., Dong, Q., Amos, C. I. & Wu, X. Genetic susceptibility to lung cancer: the role of DNA damage and repair. Cancer Epidemiol. Biomark. Prev. 12, 689–698 (2003).
Kuzmin E., et al. Systematic analysis of complex genetic interactions. Science 360, eaao1729 (2018).
pubmed: 29674565 pmcid: 6215713
Harrington, K. J. et al. Effective targeting of solid tumors in patients with locally advanced cancers by radiolabeled pegylated liposomes. Clin. Cancer Res. 7, 243–254 (2001).
pubmed: 11234875
Foucquier, J. & Guedj, M. Analysis of drug combinations: current methodological landscape. Pharm. Res. Perspect. 3, e00149 (2015).
Engler, A. C., Lee H-i & Hammond, P. T. Highly efficient “Grafting onto” a polypeptide backbone using click chemistry. Angew. Chem. Int. Ed. 48, 9334–9338 (2009).
Engler, A. C., Bonner, D. K., Buss, H. G., Cheung, E. Y. & Hammond, P. T. The synthetic tuning of clickable pH responsive cationic polypeptides and block copolypeptides. Soft Matter 7, 5627–5637 (2011).
Zhao, X., Poon, Z., Engler, A. C., Bonner, D. K. & Hammond, P. T. Enhanced stability of polymeric micelles based on postfunctionalized poly(ethylene glycol)-b-poly(gamma-propargyl L-glutamate): the substituent effect. Biomacromolecules 13, 1315–1322 (2012).
pubmed: 22376183 pmcid: 3387562
Bangham A. D., Hill M. W., Miller N. G. A. Preparation and use of liposomes as models of biological membranes. in Methods in Membrane Biology: Volume 1 (ed Korn E. D.). (Springer, US, 1974).
Batzri, S. & Korn, E. D. Single bilayer liposomes prepared without sonication. Biochem. Biophys. Acta 298, 1015–1019 (1973).
pubmed: 4738145
Trulley, P. et al. Alternative translation initiation generates a functionally distinct isoform of the stress-activated protein kinase MK2. Cell Rep. 27, 2859–2870.e2856 (2019).
pubmed: 31167133

Auteurs

Yi Wen Kong (YW)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Center for Precision Cancer Medicine, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Erik C Dreaden (EC)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Department of Pediatrics, Aflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta, Emory University School of Medicine, Atlanta, GA, 30322, USA.

Sandra Morandell (S)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Molecular Health GmbH, 69115, Heidelberg, Germany.

Wen Zhou (W)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Sanjeev S Dhara (SS)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Ganapathy Sriram (G)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Center for Precision Cancer Medicine, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Fred C Lam (FC)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Center for Precision Cancer Medicine, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Division of Neurosurgery, Hamilton General Hospital, McMaster University Faculty of Health Sciences, Hamilton, ON, L8L 2X2, Canada.

Jesse C Patterson (JC)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Center for Precision Cancer Medicine, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Mohiuddin Quadir (M)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Department of Coatings and Polymeric Materials, North Dakota State University, Fargo, USA.

Anh Dinh (A)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Kevin E Shopsowitz (KE)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Shohreh Varmeh (S)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Center for Precision Cancer Medicine, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Ömer H Yilmaz (ÖH)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Stephen J Lippard (SJ)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

H Christian Reinhardt (HC)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Clinic I of Internal Medicine, University Hospital Cologne, Cologne, Germany.
Cologne Excellence Cluster in Cellular Stress Response in Aging-Associated Disorders (CECAD), University of Cologne, Cologne, Germany.
Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.

Michael T Hemann (MT)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Center for Precision Cancer Medicine, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Paula T Hammond (PT)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. hammond@mit.edu.
Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. hammond@mit.edu.

Michael B Yaffe (MB)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. myaffe@mit.edu.
Center for Precision Cancer Medicine, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. myaffe@mit.edu.
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. myaffe@mit.edu.
Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. myaffe@mit.edu.
Divisions of Surgical Oncology, Trauma, and Surgical Critical Care, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02215, USA. myaffe@mit.edu.

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