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Small Molecule MIF Modulation Enhances Ferroptosis by Impairing DNA Repair Mechanisms.

التفاصيل البيبلوغرافية
العنوان: Small Molecule MIF Modulation Enhances Ferroptosis by Impairing DNA Repair Mechanisms.
المؤلفون: Chen D; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Zhao C; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Zhang J; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Knol CWJ; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Osipyan A; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Majerníková N; Research School of Behavioural and Cognitive Neuroscience, University of Groningen, Groningen, 9713 AV, The Netherlands.; Department of Pathology and Medical Biology, University Medical Centre Groningen, University of Groningen, Groningen, 9713 GZ, The Netherlands.; Department of Molecular Pharmacology, Groningen Research Institute of Pharmacy, University of Groningen, Groningen, 9713 AV, The Netherlands., Chen T; Department of Molecular Pharmacology, Groningen Research Institute of Pharmacy, University of Groningen, Groningen, 9713 AV, The Netherlands., Xiao Z; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Adriana J; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Griffith AJ; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Gamez AS; Department of Biomedical Sciences of Cell & Systems, Section Molecular Cell Biology, University Medical Center Groningen, University of Groningen, Groningen, 9712 CP, The Netherlands.; Department of Radiation Oncology, University Medical Center Groningen, Hanzeplein 1, Groningen, 9713 GZ, Netherlands., van der Wouden PE; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Coppes RP; Department of Biomedical Sciences of Cell & Systems, Section Molecular Cell Biology, University Medical Center Groningen, University of Groningen, Groningen, 9712 CP, The Netherlands.; Department of Radiation Oncology, University Medical Center Groningen, Hanzeplein 1, Groningen, 9713 GZ, Netherlands., Dolga AM; Research School of Behavioural and Cognitive Neuroscience, University of Groningen, Groningen, 9713 AV, The Netherlands.; Department of Molecular Pharmacology, Groningen Research Institute of Pharmacy, University of Groningen, Groningen, 9713 AV, The Netherlands., Haisma HJ; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands., Dekker FJ; Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, Antonius Deusinglaan 1, Groningen, 9713 AV, The Netherlands.
المصدر: Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Adv Sci (Weinh)] 2024 Jun 25, pp. e2403963. Date of Electronic Publication: 2024 Jun 25.
Publication Model: Ahead of Print
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: WILEY-VCH Country of Publication: Germany NLM ID: 101664569 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2198-3844 (Electronic) Linking ISSN: 21983844 NLM ISO Abbreviation: Adv Sci (Weinh) Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Weinheim : WILEY-VCH, [2014]-
مستخلص: Ferroptosis is a form of regulated cell death that can be modulated by small molecules and has the potential for the development of therapeutics for oncology. Although excessive lipid peroxidation is the defining hallmark of ferroptosis, DNA damage may also play a significant role. In this study, a potential mechanistic role for MIF in homologous recombination (HR) DNA repair is identified. The inhibition or genetic depletion of MIF or other HR proteins, such as breast cancer type 1 susceptibility protein (BRCA1), is demonstrated to significantly enhance the sensitivity of cells to ferroptosis. The interference with HR results in the translocation of the tumor suppressor protein p53 to the mitochondria, which in turn stimulates the production of reactive oxygen species. Taken together, the findings demonstrate that MIF-directed small molecules enhance ferroptosis via a putative MIF-BRCA1-RAD51 axis in HR, which causes resistance to ferroptosis. This suggests a potential novel druggable route to enhance ferroptosis by targeted anticancer therapeutics in the future.
(© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.)
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معلومات مُعتمدة: 201907720019 China Scholarship Council; 202006220019 China Scholarship Council; 202107060008 China Scholarship Council; OCENW.M.21.213 Nederlandse Organisatie voor Wetenschappelijk Onderzoek; 40-00506-98-9021 Nederlandse Organisatie voor Wetenschappelijk Onderzoek; 175-010-2009-023 Nederlandse Organisatie voor Wetenschappelijk Onderzoek
فهرسة مساهمة: Keywords: DNA repair; ferroptosis; homologous recombination; inhibitor; macrophage migration inhibitory factor (MIF)
تواريخ الأحداث: Date Created: 20240626 Latest Revision: 20240626
رمز التحديث: 20240627
DOI: 10.1002/advs.202403963
PMID: 38924362
قاعدة البيانات: MEDLINE
الوصف
تدمد:2198-3844
DOI:10.1002/advs.202403963