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FEBS Lett. 2019 Jun 29. doi: 10.1002/1873-3468.13521. [Epub ahead of print]

HDAC2-dependent miRNA signature in acute myeloid leukemia.

Author information

1
IRCCS, SDN, Naples, Italy.
2
Department of Precision Medicine, University of Campania "L. Vanvitelli", Naples, Italy.

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.

KEYWORDS:

HDAC2; SAHA; epigenetics; immunoregulation; leukemia; miRNA

PMID:
31254352
DOI:
10.1002/1873-3468.13521

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