HDAC2-dependent miRNA signature in acute myeloid leukemia

Mariarosaria Conte, Carmela Dell'Aversana, Giulia Sgueglia, Annamaria Carissimo, Lucia Altucci

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)2574-2584
Number of pages11
JournalFEBS Letters
Volume593
Issue number18
DOIs
Publication statusPublished - Sep 1 2019

Keywords

  • epigenetics
  • HDAC2
  • immunoregulation
  • leukemia
  • miRNA
  • SAHA

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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  • Cite this

    Conte, M., Dell'Aversana, C., Sgueglia, G., Carissimo, A., & Altucci, L. (2019). HDAC2-dependent miRNA signature in acute myeloid leukemia. FEBS Letters, 593(18), 2574-2584. https://doi.org/10.1002/1873-3468.13521