Receptor-type tyrosine-protein phosphatase κ directly targets STAT3 activation for tumor suppression in nasal NK/T-cell lymphoma

Author:

Chen Yun-Wen1,Guo Tianhuan1,Shen Lijun1,Wong Kai-Yau1,Tao Qian2,Choi William W. L.1,Au-Yeung Rex K. H.1,Chan Yuen-Piu1,Wong Michelle L. Y.1,Tang Johnny C. O.3,Liu Wei-Ping4,Li Gan-Di4,Shimizu Norio5,Loong Florence1,Tse Eric6,Kwong Yok-Lam6,Srivastava Gopesh1

Affiliation:

1. Lymphoma Research Laboratory, Department of Pathology, Queen Mary Hospital, The University of Hong Kong, Hong Kong;

2. Cancer Epigenetics Laboratory, Department of Clinical Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong;

3. Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hong Kong;

4. Department of Pathology, West-China Hospital of Sichuan University, Chengdu, Sichuan, China;

5. Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan; and

6. Division of Hematology, Medical Oncology and Bone Marrow Transplantation, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong

Abstract

Key Points PTPRK binds to STAT3 and directly dephosphorylates phospho-STAT3 at Tyr705. Loss of PTPRK, located in the deleted 6q region, leads to STAT3 activation and contributes to nasal-type NK/T-cell lymphoma pathogenesis.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference49 articles.

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