دورية أكاديمية
أعرض في EDS

Ferroptosis response segregates small cell lung cancer (SCLC) neuroendocrine subtypes.

التفاصيل البيبلوغرافية
العنوان: Ferroptosis response segregates small cell lung cancer (SCLC) neuroendocrine subtypes.
المؤلفون: Bebber CM; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany.; Clinic I for Internal Medicine, Medical Faculty, University Hospital of Cologne, Cologne, Germany., Thomas ES; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany.; Imperial College London, London, UK., Stroh J; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany., Chen Z; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany., Androulidaki A; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany., Schmitt A; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany.; Clinic I for Internal Medicine, Medical Faculty, University Hospital of Cologne, Cologne, Germany., Höhne MN; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany.; Department for Chemistry, Institute for Biochemistry, University of Cologne, Cologne, Germany., Stüker L; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany., de Pádua Alves C; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany., Khonsari A; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; Institute of Pathology, Medical Faculty, University Hospital of Cologne, Cologne, Germany.; Center for Molecular Medicine Cologne, Medical Faculty, University Hospital of Cologne, Cologne, Germany., Dammert MA; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; Institute of Pathology, Medical Faculty, University Hospital of Cologne, Cologne, Germany.; Center for Molecular Medicine Cologne, Medical Faculty, University Hospital of Cologne, Cologne, Germany., Parmaksiz F; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; Institute of Pathology, Medical Faculty, University Hospital of Cologne, Cologne, Germany.; Center for Molecular Medicine Cologne, Medical Faculty, University Hospital of Cologne, Cologne, Germany., Tumbrink HL; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; Institute of Pathology, Medical Faculty, University Hospital of Cologne, Cologne, Germany.; Center for Molecular Medicine Cologne, Medical Faculty, University Hospital of Cologne, Cologne, Germany., Beleggia F; Clinic I for Internal Medicine, Medical Faculty, University Hospital of Cologne, Cologne, Germany., Sos ML; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; Institute of Pathology, Medical Faculty, University Hospital of Cologne, Cologne, Germany.; Center for Molecular Medicine Cologne, Medical Faculty, University Hospital of Cologne, Cologne, Germany., Riemer J; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany.; Department for Chemistry, Institute for Biochemistry, University of Cologne, Cologne, Germany., George J; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany., Brodesser S; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany., Thomas RK; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.; Institute of Pathology, Medical Faculty, University Hospital of Cologne, Cologne, Germany.; DKFZ, German Cancer Research Center, German Cancer Consortium (DKTK), Heidelberg, Germany., Reinhardt HC; Department of Hematology and Stem Cell Transplantation, University Hospital Essen, University Duisburg-Essen, German Cancer Consortium (DKTK partner site Essen), Essen, Germany., von Karstedt S; Department of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany. s.vonkarstedt@uni-koeln.de.; CECAD Cluster of Excellence, University of Cologne, Cologne, Germany. s.vonkarstedt@uni-koeln.de.; Center for Molecular Medicine Cologne, Medical Faculty, University Hospital of Cologne, Cologne, Germany. s.vonkarstedt@uni-koeln.de.
المصدر: Nature communications [Nat Commun] 2021 Apr 06; Vol. 12 (1), pp. 2048. Date of Electronic Publication: 2021 Apr 06.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Ferroptosis*, Neuroendocrine Tumors/*pathology , Small Cell Lung Carcinoma/*pathology, Animals ; Antioxidants/metabolism ; Apoptosis ; Biomarkers, Tumor/metabolism ; Cell Line, Tumor ; Cell Survival ; Humans ; Lipid Metabolism ; Male ; Mice, Nude ; Models, Biological ; Necroptosis ; Phospholipid Hydroperoxide Glutathione Peroxidase/metabolism ; Phospholipids/metabolism ; Prognosis ; Thioredoxins/metabolism ; Mice
مستخلص: Loss of TP53 and RB1 in treatment-naïve small cell lung cancer (SCLC) suggests selective pressure to inactivate cell death pathways prior to therapy. Yet, which of these pathways remain available in treatment-naïve SCLC is unknown. Here, through systemic analysis of cell death pathway availability in treatment-naïve SCLC, we identify non-neuroendocrine (NE) SCLC to be vulnerable to ferroptosis through subtype-specific lipidome remodeling. While NE SCLC is ferroptosis resistant, it acquires selective addiction to the TRX anti-oxidant pathway. In experimental settings of non-NE/NE intratumoral heterogeneity, non-NE or NE populations are selectively depleted by ferroptosis or TRX pathway inhibition, respectively. Preventing subtype plasticity observed under single pathway targeting, combined treatment kills established non-NE and NE tumors in xenografts, genetically engineered mouse models of SCLC and patient-derived cells, and identifies a patient subset with drastically improved overall survival. These findings reveal cell death pathway mining as a means to identify rational combination therapies for SCLC.
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المشرفين على المادة: 0 (Antioxidants)
0 (Biomarkers, Tumor)
0 (Phospholipids)
52500-60-4 (Thioredoxins)
EC 1.11.1.12 (Phospholipid Hydroperoxide Glutathione Peroxidase)
تواريخ الأحداث: Date Created: 20210407 Date Completed: 20210414 Latest Revision: 20240226
رمز التحديث: 20240226
مُعرف محوري في PubMed: PMC8024350
DOI: 10.1038/s41467-021-22336-4
PMID: 33824345
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-021-22336-4