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LIFRα-CT3 induces differentiation of a human acute myelogenous leukemia cell line HL-60 by suppressing miR-155 expression through the JAK/STAT pathway.

Abstract
The distal cytoplasmic motifs of the leukemia inhibitory factor receptor α-chain (LIFRα-CT3) and its TAT fusion protein (TAT-CT3) can independently suppress cell viability and induce myeloid differentiation in human leukemia HL-60 cells in our previous studies. But its underlying mechanism remains undefined. Herein, we show that a prokaryotic expressed TAT-CT3 induced a rapid elevation of STAT3 phosphorylation (pSTAT3), and then suppress the transcription of miR-155 and induce the elevation of SOCS-1, which further inhibited STAT3 phosphorylation for a long-term period. Our result indicated a novel mechanism of TAT-CT3 to promote HL60 cells differentiation, which provides some potential therapeutic targets for future acute myelogenous leukemia therapy.
AuthorsSha Xu, Zhenyu Xu, Baohai Liu, Qing Sun, Ling Yang, Jianmin Wang, Yue Wang, Houqi Liu
JournalLeukemia research (Leuk Res) Vol. 38 Issue 10 Pg. 1237-44 (Oct 2014) ISSN: 1873-5835 [Electronic] England
PMID25092123 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2014 Elsevier Ltd. All rights reserved.
Chemical References
  • LIFR protein, human
  • Leukemia Inhibitory Factor Receptor alpha Subunit
  • MIRN155 microRNA, human
  • MicroRNAs
  • Oncogene Proteins, Fusion
  • STAT Transcription Factors
  • Janus Kinases
Topics
  • Blotting, Western
  • Cell Differentiation (physiology)
  • Chromatin Immunoprecipitation
  • Flow Cytometry
  • Gene Expression Regulation, Neoplastic (physiology)
  • HL-60 Cells
  • Humans
  • Janus Kinases (metabolism)
  • Leukemia Inhibitory Factor Receptor alpha Subunit (genetics, metabolism)
  • Leukemia, Myeloid, Acute (genetics, metabolism)
  • MicroRNAs (biosynthesis, genetics)
  • Oncogene Proteins, Fusion (genetics, metabolism)
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • STAT Transcription Factors (metabolism)
  • Signal Transduction (physiology)

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