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CDK9 Inhibitor Induces the Apoptosis of B-Cell Acute Lymphocytic Leukemia by Inhibiting c-Myc-Mediated Glycolytic Metabolism

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单位： [1]Department of Pathology, School of Basic Medical Science, Central South University, Changsha, China, [2]Departmentof Pathology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China, [3]Key Laboratory of Pediatric Hematology and Oncology, Shanghai Children’s Medical Center, Ministry of Health, Pediatric TranslationalMedicine Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, China, [4]Department of Gynecology and Obstetrics, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, China, [5]Shanghai CollaborativeInnovation Center for Translational Medicine, Department of Pharmacology and Chemical Biology, Shanghai Jiao TongUniversity School of Medicine, Shanghai, China, [6]State Key Laboratory of Medical Genomics, National Research Centerfor Translational Medicine at Shanghai, Shanghai Institute of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao TongUniversity School of Medicine, Shanghai, China, [7]Department of Pathophysiology, School of Basic Medical Sciences,Wuhan University, Wuhan, China

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关键词： B-cell acute lymphocytic leukemia c-Myc CDK9 inhibitors cell apoptosis glycolysis

摘要：

B-cell acute lymphocytic leukemia (B-ALL), a common blood cancer in children, leads to high mortality. Cyclin-dependent kinase 9 inhibitor (CDK9i) effectively attenuates acute myeloid leukemia and chronic lymphoblastic leukemia by inducing apoptosis and inhibiting cell proliferation. However, the effect of CDK9i on B-ALL cells and the underlying mechanisms remain unclear. In this study, we showed that CDK9i induced the apoptosis of B-ALL cells in vitro by activating the apoptotic pathways. In addition, CDK9i restrained the glycolytic metabolism of B-ALL cells, and CDK9i-induced apoptosis was enhanced by co-treatment with glycolysis inhibitors. Furthermore, CDK9i restained the glycolysis of B-ALL cell lines by markedly downregulating the expression of glucose transporter type 1 (GLUT1) and the key rate-limiting enzymes of glycolysis, such as hexokinase 2 (HK2) and lactate dehydrogenase A (LDHA). Moreover, cell apoptosis was rescued in B-ALL cells with over-expressed c-Myc after treatment with CDK9i, which is involved in the enhancement of glycolytic metabolism. In summary, our findings suggest that CDK9 inhibitors induce the apoptosis of B-ALL cells by inhibiting c-Myc-mediated glycolytic metabolism, thus providing a new strategy for the treatment of B-ALL. © Copyright © 2021 Huang, Abudureheman, Xia, Chu, Zhou, Zheng, Zhou, Shi, Li, Zhu, Qing, Ji, Liang, Guo, Yin and Duan.

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出版当年[2020]版中科院分区表Review为是的期刊

：

大类 | 2 区生物

小类 | 2 区发育生物学 3 区细胞生物学

最新[2025]版：

大类 | 2 区生物学

小类 | 2 区发育生物学 3 区细胞生物学

第一作者：

第一作者单位： [1]Department of Pathology, School of Basic Medical Science, Central South University, Changsha, China, [2]Departmentof Pathology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China,

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通讯作者：

通讯机构： [2]Departmentof Pathology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China, [3]Key Laboratory of Pediatric Hematology and Oncology, Shanghai Children’s Medical Center, Ministry of Health, Pediatric TranslationalMedicine Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, China, [5]Shanghai CollaborativeInnovation Center for Translational Medicine, Department of Pharmacology and Chemical Biology, Shanghai Jiao TongUniversity School of Medicine, Shanghai, China,

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CDK9 Inhibitor Induces the Apoptosis of B-Cell Acute Lymphocytic Leukemia by Inhibiting c-Myc-Mediated Glycolytic Metabolism

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