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UBC9 Deficiency Accelerates AML Progression By Downregulating PARP1 Sumoylation and Subsequently Activating the NF-κB Pathway

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单位: [1]Department of Hematology, Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China, Wuhan, China [2] tongji hospital, wuhan, China [3]Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China, Wuhan, China [4]Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, wuhan, China [5]Department of Hematology, Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China, wuhan, Chin
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Acute myeloid leukemia (AML) is the most common acute leukemia in adults and is a disease of heterogeneous clonal hematopoietic progenitor cells. Despite the relentless development of therapeutic options, including chemotherapy, and identication of many new therapeutic targets, the prognosis of AML is still poor, with a 5-year survival rate of approximately 35% in patients younger than 60 years old and 10% in patients older than 60 years, which may be due to the high degree of AML heterogeneity. Targeting the shared mechanisms of action among subclones has emerged led to nd novel strategies, such as targeting protein post post-translational modication. Here we show that the impact of the UBC9 (the only E2 conjugation enzyme) and its related SUMOylation, a critical and reversible posttranslational modication as ubiquitination, on AML progression, to provide novel and potent sight for AML therapy.

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出版当年[2022]版:
大类 | 1 区 医学
小类 | 1 区 血液学
最新[2025]版:
大类 | 1 区 医学
小类 | 1 区 血液学
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出版当年[2021]版:
Q1 HEMATOLOGY
最新[2023]版:
Q1 HEMATOLOGY

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第一作者单位: [1]Department of Hematology, Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China, Wuhan, China
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