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.
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Authors | Sha Xu, Zhenyu Xu, Baohai Liu, Qing Sun, Ling Yang, Jianmin Wang, Yue Wang, Houqi Liu |
Journal | Leukemia research
(Leuk Res)
Vol. 38
Issue 10
Pg. 1237-44
(Oct 2014)
ISSN: 1873-5835 [Electronic] England |
PMID | 25092123
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 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
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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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