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Vol 57(2023) N 4 p. 653-660; DOI 10.1134/S0026893323040179  M.-Xi Wang1,2, S.-He Yu1, M. Xiao3*, J. Chen1** JMJD3 Exerts Oncorepressor Activity in Acute Promyelocytic Leukemia by Promoting PU.1 Expression 1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025 China2Department of Hematology, Xuzhou Central Hospital, Xuzhou Medical University, Xuzhou, 221009 China 3Shanghai Ji Ai Genetics and IVF Institute, the Obstetrics and Gynecology Hospital of Fudan University, Shanghai, 200011 China *xiaomin3296@163.com **chenjuanrj@163.com Received - 2022-08-27; Revised - 2022-11-02; Accepted - 2022-11-03 All-trans retinoic acid (ATRA) in acute promyelocytic leukemia (APL) has been the most famous differentiation induction therapy during which the expression of PU.1, a key transcription factor (TF) for myeloid lineage determination in normal hematopoiesis is restored. In our previous studies, we found a stress-inducible H3K27 demethylase, JMJD3, to directly upregulate PU.1 expression to promote myeloid commitment during normal myelopoiesis. In addition, JMJD3 acts as an oncorepressor and plays a critical regulatory role in the initiation and progression of malignant hematopoiesis. In this study, we further resolved the relationship between JMJD3 and PU.1 in APL therein JMJD3 exerts oncorepressor activity via promoting PU.1 expression. acute myeloid leukemia, histone demethylase, JMJD3, PU.1, myeloid differentiation |
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