HDAC2-dependent miRNA signature in acute myeloid leukemia.
FEBS Lett
; 593(18): 2574-2584, 2019 09.
Article
em En
| MEDLINE
| ID: mdl-31254352
ABSTRACT
Acute myeloid leukemia (AML) arises from a complex sequence of biological and finely orchestrated events that are still poorly understood. Increasingly, epigenetic studies are providing exciting findings that may be exploited in promising and personalized cutting-edge therapies. A more appropriate and broader screening of possible players in cancer could identify a master molecular mechanism in AML. Here, we build on our previously published study by evaluating a histone deacetylase (HDAC)2-mediated miRNA regulatory network in U937 leukemic cells. Following a comparative miRNA profiling analysis in genetically and enzymatically HDAC2-downregulated AML cells, we identified miR-96-5p and miR-92a-3p as potential regulators in AML etiopathology by targeting defined genes. Our findings support the potentially beneficial role of alternative physiopathological interventions.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Leucemia Mieloide Aguda
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MicroRNAs
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Histona Desacetilase 2
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Revista:
FEBS Lett
Ano de publicação:
2019
Tipo de documento:
Article