MicroRNA-155 expression and function in AML: An evolving paradigm

被引:24
|
作者
Narayan, Nisha [1 ]
Bracken, Cameron P. [2 ,3 ]
Ekert, Paul G. [1 ]
机构
[1] Murdoch Childrens Res Inst, 50 Flemington Rd, Parkville, Vic 3052, Australia
[2] SA Pathol, Ctr Canc Biol, Adelaide, SA 5000, Australia
[3] Univ South Australia, Adelaide, SA 5000, Australia
基金
英国医学研究理事会;
关键词
ACUTE MYELOID-LEUKEMIA; B-CELL LYMPHOMAS; STEM-CELLS; TRANSCRIPTION FACTOR; MOLECULAR LANDSCAPE; HEMATOPOIETIC-CELLS; MIR-155; GENE; PU.1; TARGET;
D O I
10.1016/j.exphem.2018.03.007
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acute myeloid leukemia (AML) arises when immature myeloid blast cells acquire multiple, recurrent genetic and epigenetic changes that result in dysregulated proliferation. Acute leukemia is the most common form of pediatric cancer, with AML accounting for similar to 20% of all leukemias in children. The genomic aberrations that drive AML inhibit myeloid differentiation and activate signal transduction pathways that drive proliferation. MicroRNAs, a class of small (similar to 22 nucleotide) noncoding RNAs that posttranscriptionally suppress the expression of specifically targeted transcripts, are also frequently dysregulated in AML, which may prove useful for the purposes of disease classification, prognosis, and future therapeutic approaches. MicroRNA expression profiles are associated with patient prognosis and responses to standard chemotherapy, including predicting therapy resistance in AML. miR-155 is the primary focus of this review because it has been repeatedly associated with poorer survival across multiple cohorts of adult and pediatric AML. We discuss some novel features of miR-155 expression in AML, in particular how the levels of expression can critically influence function. Understanding the role of microRNAs in AML and the ways in which microRNA expression influences AML biology is one means to develop novel and more targeted therapies. (C) 2018 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:1 / 6
页数:6
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