miR-125b promotes MLL-AF9–driven murine acute myeloid leukemia involving a VEGFA-mediated non–cell-intrinsic mechanism

Author:

Liu Jun12,Guo Bo123,Chen Zhuo124,Wang Nayi124,Iacovino Michelina5,Cheng Jijun12,Roden Christine12,Pan Wen12,Khan Sajid6,Chen Suning7,Kyba Michael8,Fan Rong24,Guo Shangqin25,Lu Jun129

Affiliation:

1. Department of Genetics, Yale University School of Medicine, New Haven, CT;

2. Yale Stem Cell Center, Yale Cancer Center, New Haven, CT;

3. Chinese People's Liberation Army General Hospital, Beijing, China;

4. Department of Biomedical Engineering, Yale University, New Haven, CT;

5. Department of Cell Biology, and

6. Department of Surgery, Yale University School of Medicine, New Haven, CT;

7. Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China;

8. Lillehei Heart Institute and Department of Pediatrics, University of Minnesota, Minneapolis, MN; and

9. Yale Center for RNA Science and Medicine, New Haven, CT

Abstract

Key Points miR-125b overexpression accelerates MLL-AF9–driven AML and endows partial addiction to its overexpression. A miR-125b-TET2-VEGFA pathway promotes leukemogenesis involving a non–cell-intrinsic mechanism.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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