期刊
EXPERIMENTAL HEMATOLOGY
卷 58, 期 -, 页码 44-51出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.exphem.2017.10.002
关键词
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资金
- Council of Scientific and Industrial Research (CSIR) (NWP/BIODISCOVERY) [BSC 0120]
- Department of Biotechnology (DBT) [BT/PR13023/MED/31/311/2015]
- Ramalingaswami fellowship [BT/RLF/RE-ENTRY/06/2010]
- Department of Science and Technology of the Government of India [SB/SO/HS-053/2013]
- CSIR-Shyama Prasad Mukherjee (SPM) fellowship [SPM-31/002(0206)/2014-EMR-I]
- CSIR
Acute myeloid leukemia (AML) remains an aggressive hematopoietic malignancy that is caused by proliferation of immature myeloid cells and is frequently characterized by perturbations in chromatin -modifying enzymes. Emerging evidence indicates that histone demethylases play a role in tumorigenesis. However, due to the complexity of this enormous family of histone-modifying enzymes, substrate redundancy, and context-specific roles, the contribution of each member remains ambiguous and targeting them remains challenging. Here, we analyzed expression of histone-3-lysine (H3K) demethylases and their cognate substrates in a cohort of de novo AML patients, which demonstrated that the expression of H3K27Me3/2-demethylases and selected members of H3K9Me3/2/1-demethylases are significantly increased in AML. KDM6 upregulation is associated with a global decrease in H3K27Me3 level. Importantly, our data show that pharmacological inhibition of H3K27Me3/2-demethylases or H3K9Me3/2-demethylases, either alone or in combination, could be considered an interesting molecular therapeutic modality in human AML independent of its subtype. (C) 2018 ISEH Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
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