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CYB561A3 is the Key Lysosomal Iron Reductase Required for Burkitt B-cell Growth and Survival.

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机构： [1]Division of Infectious Diseases, Department of Medicine, Brigham and Women’s Hospital, 181 Longwood Avenue, Boston MA 02115, USA [2]Broad Institute of Harvard and MIT, Cambridge, MA 02142, United States of America [3]Department of Microbiology, Harvard Medical School, Boston, MA 02115, USA [4]Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of China [5]Howard Hughes Medical Institute and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02115 USA [6]Present address, Department of Cancer Physiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA [7]Department of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA

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关键词： iron metabolism ascorbate transferrin lymphocyte lymphoma iron-sulfur cluster CRISPR screen reactive oxygen species Cytochrome 561 HIF1 alpha ferroptosis

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Epstein-Barr virus (EBV) causes endemic Burkitt lymphoma, the leading childhood cancer in sub-Saharan Africa. Burkitt cells retain aspects of germinal center B-cell physiology with MYC-driven B-cell hyperproliferation, yet little is presently known about their iron metabolism. CRISPR/Cas9 analysis highlighted the little studied ferrireductase CYB561A3 as critical for Burkitt proliferation, but not for that of closely related EBV-transformed lymphoblastoid cells or nearly all other Cancer Dependency Map cell lines. Burkitt CYB561A3 knockout induced profound iron starvation, despite ferritinophagy and plasma membrane transferrin upregulation. Elevated concentrations of ascorbic acid, a key CYB561 family electron donor or the labile iron source ferrous citrate rescued Burkitt CYB561A3 deficiency. CYB561A3 knockout caused catastrophic lysosomal and mitochondrial damage and impaired mitochondrial respiration. By contrast, lymphoblastoid B-cells with the transforming EBV latency III program were instead dependent on the STEAP3 ferrireductase. These results highlight CYB561A3 it as an attractive therapeutic Burkitt lymphoma target.Copyright © 2021 American Society of Hematology.

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出版当年[2021]版：

大类 | 1 区

医学

小类 | 1 区血液学

最新[2023]版：

大类 | 1 区

医学

小类 | 1 区血液学

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第一作者机构： [1]Division of Infectious Diseases, Department of Medicine, Brigham and Women’s Hospital, 181 Longwood Avenue, Boston MA 02115, USA [2]Broad Institute of Harvard and MIT, Cambridge, MA 02142, United States of America [3]Department of Microbiology, Harvard Medical School, Boston, MA 02115, USA [4]Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of China

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通讯机构： [1]Division of Infectious Diseases, Department of Medicine, Brigham and Women’s Hospital, 181 Longwood Avenue, Boston MA 02115, USA [2]Broad Institute of Harvard and MIT, Cambridge, MA 02142, United States of America [3]Department of Microbiology, Harvard Medical School, Boston, MA 02115, USA

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CYB561A3 is the Key Lysosomal Iron Reductase Required for Burkitt B-cell Growth and Survival.

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