Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/23305
Title: Receptor-type tyrosine-protein phosphatase £e directly targets STAT3 activation for tumor suppression in nasal NK/T-cell lymphoma
Authors: Chen, YW
Guo, T
Shen, L
Wong, KY
Tao, Q
Choi, WW
Au-Yeung, RK
Chan, YP
Wong, ML
Tang, JC 
Liu, WP
Li, GD
Shimizu, N
Loong, F
Tse, E
Kwong, YL
Srivastava, G
Issue Date: 2015
Publisher: American Society of Hematology
Source: Blood, 2015, v. 125, no. 10, p. 1589-1600 How to cite?
Journal: Blood 
Abstract: Nasal-type natural killer/T-cell lymphoma (NKTCL) is an aggressive disease characterized by frequent deletions on 6q, and constitutive activation of signal transducer and activator of transcription 3 (STAT3). Phosphorylation at Tyr705 activates STAT3, inducing dimerization, nuclear translocation, and DNA binding. In this study, we investigated whether receptor-type tyrosine-protein phosphatase £e (PTPRK), the only protein tyrosine phosphatase at 6q that contains a STAT3-specifying motif, negatively regulates STAT3 activation in NKTCL. PTPRK was highly expressed in normal NK cells but was underexpressed in 4 of 5 (80%) NKTCL cell lines and 15 of 27 (55.6%) primary tumors. Significantly, PTPRK protein expression was inversely correlated with nuclear phospho-STAT3(Tyr705) expression in NKTCL cell lines (P = .025) and tumors (P = .040). PTPRK restoration decreased nuclear phospho-STAT3(Tyr705) levels, whereas knockdown of PTPRK increased such levels in NKTCL cells. Phosphatase substrate-trapping mutant assays demonstrated the binding of PTPRK to STAT3, and phosphatase assays showed t
URI: http://hdl.handle.net/10397/23305
ISSN: 0006-4971
EISSN: 1528-0020
DOI: 10.1182/blood-2014-07-588970
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