EZH2 phosphorylation by JAK3 mediates a switch to noncanonical function in natural killer/T-cell lymphoma

Author:

Yan Junli1,Li Boheng2,Lin Baohong3,Lee Pei Tsung1,Chung Tae-Hoon1,Tan Joy1,Bi Chonglei1,Lee Xue Ting1,Selvarajan Viknesvaran4,Ng Siok-Bian124,Yang Henry1,Yu Qiang5,Chng Wee-Joo123

Affiliation:

1. Cancer Science Institute of Singapore, and

2. Yong Loo Lin School of Medicine, National University of Singapore, Singapore;

3. Department of Haematology-Oncology, National University Cancer Institute of Singapore, and

4. Department of Pathology, National University Health System, Singapore;

5. Department of Cancer Biology and Pharmacology, Genome Institute of Singapore, Agency for Science, Technology, and Research (A*STAR), Biopolis, Singapore

Abstract

Key Points JAK3-mediated phosphorylation of EZH2 resulted in EZH2 oncogenic function independent of its enzymatic activity. Targeted inhibition of JAK3 may be a promising treatment in NK/TL through suppressing noncanonical EZH2 activity.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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