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Updated: Mar 20, 2026

Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation
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Expression and Function of Histone Deacetylase 10 (HDAC10) in B Cell Malignancies

John Powers1,2, Maritza Lienlaf1, Patricio Perez-Villarroel1

  • 1Department of Immunology, H. Lee Moffitt Cancer Center & Research Institute, SRB-2 Room 22344A2, 12902 Magnolia Drive, Tampa, FL, USA.

Methods in Molecular Biology (Clifton, N.J.)
|June 2, 2016
PubMed

Insights

Overexpressing Histone deacetylase 10 (HDAC10) in aggressive B cell lymphomas induced rapid cell death and cell cycle arrest. This suggests HDAC10’s potential role in targeting malignant cells.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Histone deacetylase 10 (HDAC10) is a class IIb enzyme with an uncharacterized biological role.
  • Reduced HDAC10 expression is observed in aggressive solid tumors, hinting at its tumor-suppressive function.
  • The role of HDAC10 in B cell malignancies like mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL) is largely unknown.

Purpose of the Study:

  • To investigate the function of HDAC10 in B cell malignancies.
  • To explore the therapeutic potential of HDAC10 modulation in MCL and CLL.

Main Methods:

  • Overexpression of HDAC10 in MCL (Z138c) and CLL (MEC1) cell lines.
  • Assessment of cell viability and cell cycle progression.
  • Analysis of co-stimulatory molecule expression.

Main Results:

  • HDAC10 overexpression led to rapid cell death in MCL and CLL cells within 48 hours (only 5% viability).
  • HDAC10 induction caused cell cycle arrest in these malignant B cells.
  • Co-stimulatory molecule expression was significantly upregulated following HDAC10 overexpression.

Conclusions:

  • HDAC10 functions as a tumor suppressor in B cell malignancies.
  • Targeting HDAC10 may represent a novel therapeutic strategy for MCL and CLL.
  • Further studies are warranted to elucidate the precise mechanisms of HDAC10 action in these cancers.
Keywords:
Adenoviral overexpressionGenotypingHigh-throughput flow screeningHistone deacetylase 10PCRWestern blottingqRT-PCR

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