دورية أكاديمية
أعرض في EDS

Non-cell-autonomous cancer progression from chromosomal instability.

التفاصيل البيبلوغرافية
العنوان: Non-cell-autonomous cancer progression from chromosomal instability.
المؤلفون: Li J; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Hubisz MJ; Department of Physiology, Biophysics, and Systems Biology, Weill Cornell Medicine, New York, NY, USA.; Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.; Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA.; Bioinformatics Facility, Institute of Biotechnology, Cornell University, Ithaca, NY, USA., Earlie EM; Department of Physiology, Biophysics, and Systems Biology, Weill Cornell Medicine, New York, NY, USA.; Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.; Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA., Duran MA; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Hong C; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Varela AA; Department of Physiology, Biophysics, and Systems Biology, Weill Cornell Medicine, New York, NY, USA.; Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.; Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA., Lettera E; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Deyell M; Department of Physiology, Biophysics, and Systems Biology, Weill Cornell Medicine, New York, NY, USA.; Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.; Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA., Tavora B; Volastra Therapeutics Inc., New York, NY, USA., Havel JJ; Volastra Therapeutics Inc., New York, NY, USA., Phyu SM; Department of Oncology, Medical Sciences Division, University of Oxford, Oxford, UK., Amin AD; Columbia Center for Translational Immunology, New York, NY, USA.; Division of Hematology and Oncology, Columbia University Medical Center, New York, NY, USA., Budre K; Department of Physiology, Biophysics, and Systems Biology, Weill Cornell Medicine, New York, NY, USA.; Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.; Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA., Kamiya E; Department of Physiology, Biophysics, and Systems Biology, Weill Cornell Medicine, New York, NY, USA.; Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.; Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA., Cavallo JA; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Garris C; Department of Pathology, Harvard Medical School, Boston, MA, USA.; Center for Systems Biology, Massachusetts General Hospital, Boston, MA, USA., Powell S; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Reis-Filho JS; Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Wen H; Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Bettigole S; Volastra Therapeutics Inc., New York, NY, USA., Khan AJ; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Izar B; Columbia Center for Translational Immunology, New York, NY, USA.; Division of Hematology and Oncology, Columbia University Medical Center, New York, NY, USA., Parkes EE; Department of Oncology, Medical Sciences Division, University of Oxford, Oxford, UK., Laughney AM; Department of Physiology, Biophysics, and Systems Biology, Weill Cornell Medicine, New York, NY, USA. ashley.laughney@gmail.com.; Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA. ashley.laughney@gmail.com.; Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA. ashley.laughney@gmail.com., Bakhoum SF; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. samuel.bakhoum@gmail.com.; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA. samuel.bakhoum@gmail.com.
المصدر: Nature [Nature] 2023 Aug; Vol. 620 (7976), pp. 1080-1088. Date of Electronic Publication: 2023 Aug 23.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 0410462 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-4687 (Electronic) Linking ISSN: 00280836 NLM ISO Abbreviation: Nature Subsets: MEDLINE
أسماء مطبوعة: Publication: Basingstoke : Nature Publishing Group
Original Publication: London, Macmillan Journals ltd.
مواضيع طبية MeSH: Chromosomal Instability* , Disease Progression* , Neoplasms*/genetics , Neoplasms*/immunology , Neoplasms*/pathology, Humans ; Benchmarking ; Cell Communication ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/pathology ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/immunology ; Melanoma/pathology ; Tumor Microenvironment ; Interferon Type I/immunology ; Neoplasm Metastasis ; Endoplasmic Reticulum Stress ; Signal Transduction ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/immunology ; Triple Negative Breast Neoplasms/pathology
مستخلص: Chromosomal instability (CIN) is a driver of cancer metastasis 1-4 , yet the extent to which this effect depends on the immune system remains unknown. Using ContactTracing-a newly developed, validated and benchmarked tool to infer the nature and conditional dependence of cell-cell interactions from single-cell transcriptomic data-we show that CIN-induced chronic activation of the cGAS-STING pathway promotes downstream signal re-wiring in cancer cells, leading to a pro-metastatic tumour microenvironment. This re-wiring is manifested by type I interferon tachyphylaxis selectively downstream of STING and a corresponding increase in cancer cell-derived endoplasmic reticulum (ER) stress response. Reversal of CIN, depletion of cancer cell STING or inhibition of ER stress response signalling abrogates CIN-dependent effects on the tumour microenvironment and suppresses metastasis in immune competent, but not severely immune compromised, settings. Treatment with STING inhibitors reduces CIN-driven metastasis in melanoma, breast and colorectal cancers in a manner dependent on tumour cell-intrinsic STING. Finally, we show that CIN and pervasive cGAS activation in micronuclei are associated with ER stress signalling, immune suppression and metastasis in human triple-negative breast cancer, highlighting a viable strategy to identify and therapeutically intervene in tumours spurred by CIN-induced inflammation.
(© 2023. The Author(s).)
التعليقات: Comment in: Cell Res. 2024 Jan;34(1):7-8. doi: 10.1038/s41422-023-00876-2. (PMID: 37739994)
Comment in: Mol Biomed. 2024 Jan 23;5(1):4. doi: 10.1186/s43556-023-00166-8. (PMID: 38253764)
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معلومات مُعتمدة: R37 CA258829 United States CA NCI NIH HHS; R01 CA280414 United States CA NCI NIH HHS; R21 CA263381 United States CA NCI NIH HHS; R01 CA280572 United States CA NCI NIH HHS; R21 CA266660 United States CA NCI NIH HHS; DP5 OD026395 United States OD NIH HHS; P30 CA008748 United States CA NCI NIH HHS; P50 CA247749 United States CA NCI NIH HHS; United Kingdom WT_ Wellcome Trust; R01 CA266446 United States CA NCI NIH HHS; T32 GM132083 United States GM NIGMS NIH HHS; R01 CA256188 United States CA NCI NIH HHS; U01 CA210152 United States CA NCI NIH HHS
المشرفين على المادة: EC 2.7.7.- (cGAS protein, human)
0 (STING1 protein, human)
0 (Interferon Type I)
تواريخ الأحداث: Date Created: 20230823 Date Completed: 20230914 Latest Revision: 20240722
رمز التحديث: 20240722
مُعرف محوري في PubMed: PMC10468402
DOI: 10.1038/s41586-023-06464-z
PMID: 37612508
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-4687
DOI:10.1038/s41586-023-06464-z