دورية أكاديمية
JunD reduces tumor angiogenesis by protecting cells from oxidative stress.
| العنوان: | JunD reduces tumor angiogenesis by protecting cells from oxidative stress. |
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| المؤلفون: | Gerald, Damien, Berra, Edurne, Frapart, Yves M, Chan, Denise A, Giaccia, Amato J, Mansuy, Daniel, Pouysségur, Jacques, Yaniv, Moshe, Mechta-Grigoriou, Fatima |
| المساهمون: | Expression Génétique et Maladies, Institut Pasteur Paris (IP)-Centre National de la Recherche Scientifique (CNRS), Institut de signalisation, biologie du développement et cancer - Institute of Developmental Biology and Cancer (IBDC), Université Nice Sophia Antipolis (1965 - 2019) (UNS)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UniCA), Laboratoire de Chimie et de Biochimie Pharmacologiques et Toxicologiques (LCBPT - UMR 8601), Université Paris Descartes - Paris 5 (UPD5)-Institut de Chimie - CNRS Chimie (INC-CNRS)-Centre National de la Recherche Scientifique (CNRS), Department of Radiation Oncology Stanford, Stanford Medicine, Stanford University-Stanford University |
| المصدر: | ISSN: 0092-8674. |
| بيانات النشر: | HAL CCSD Elsevier |
| سنة النشر: | 2004 |
| المجموعة: | HAL Université Côte d'Azur |
| مصطلحات موضوعية: | MESH: Animals, MESH: Antioxidants, MESH: Oxidative Stress, MESH: Procollagen-Proline Dioxygenase, MESH: Proto-Oncogene Proteins c-jun, MESH: Reactive Oxygen Species, MESH: Transcription Factors, MESH: Up-Regulation, MESH: Vascular Endothelial Growth Factor A, MESH: ras Proteins, MESH: Dioxygenases, MESH: Gene Expression Regulation, Neoplastic, MESH: Humans, MESH: Hydrogen Peroxide, MESH: Hypoxia-Inducible Factor 1, alpha Subunit, MESH: Iron, MESH: Neoplasms, MESH: Neovascularization, Pathologic, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology |
| الوصف: | International audience ; Reactive oxygen species (ROS) are implicated in the pathophysiology of various diseases, including cancer. In this study, we show that JunD, a member of the AP-1 family of transcription factors, reduces tumor angiogenesis by limiting Ras-mediated production of ROS. Using junD-deficient cells, we demonstrate that JunD regulates genes involved in antioxidant defense, H2O2 production, and angiogenesis. The accumulation of H2O2 in junD-/- cells decreases the availability of FeII and reduces the activity of HIF prolyl hydroxylases (PHDs) that target hypoxia-inducible factors-alpha (HIFalpha) for degradation. Subsequently, HIF-alpha proteins accumulate and enhance the transcription of VEGF-A, a potent proangiogenic factor. Our study uncovers the mechanism by which JunD protects cells from oxidative stress and exerts an antiangiogenic effect. Furthermore, we provide new insights into the regulation of PHD activity, allowing immediate reactive adaptation to changes in O2 or iron levels in the cell. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| العلاقة: | info:eu-repo/semantics/altIdentifier/pmid/15369676; hal-00322373; https://hal.science/hal-00322373Test; PUBMED: 15369676 |
| DOI: | 10.1016/j.cell.2004.08.025 |
| الإتاحة: | https://doi.org/10.1016/j.cell.2004.08.025Test https://hal.science/hal-00322373Test |
| رقم الانضمام: | edsbas.6EDBA501 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1016/j.cell.2004.08.025 |
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