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Related Experiment Video

Updated: Jul 5, 2026

Assays for Validating Histone Acetyltransferase Inhibitors

Assays for Validating Histone Acetyltransferase Inhibitors

Published on: August 6, 2020

Mechanism for the decrease in the FIP1L1-PDGFRalpha protein level in EoL-1 cells by histone deacetylase inhibitors.

Kenji Ishihara¹, Motoko Kaneko, Hajime Kitamura

¹Laboratory of Pathophysiological Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan. ishihara@wadalab.mech.tohoku.ac.jp

International Archives of Allergy and Immunology

|June 25, 2008

Summary

Histone deacetylase (HDAC) inhibitors like apicidin decrease FIP1L1-PDGFRalpha protein levels in leukemia cells. This reduction is linked to decreased translation, not mRNA levels, suggesting a novel therapeutic mechanism.

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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

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

Published on: September 20, 2017

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Last Updated: Jul 5, 2026

Assays for Validating Histone Acetyltransferase Inhibitors

Assays for Validating Histone Acetyltransferase Inhibitors

Published on: August 6, 2020

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

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

Published on: September 20, 2017

Area of Science:

Biochemistry
Molecular Biology
Cancer Research

Background:

Protein acetylation and deacetylation are regulated by histone acetyltransferase and histone deacetylase (HDAC).
EoL-1 leukemia cells harbor the FIP1L1-PDGFRA fusion gene, driving oncogenesis.
HDAC inhibitors apicidin and n-butyrate reduce FIP1L1-PDGFRalpha protein levels, inducing differentiation in EoL-1 cells.

Purpose of the Study:

To elucidate the mechanism by which apicidin and n-butyrate decrease FIP1L1-PDGFRalpha protein levels in EoL-1 cells.

Main Methods:

EoL-1 cells were treated with HDAC inhibitors (apicidin, trichostatin A, n-butyrate).
Protein levels of FIP1L1-PDGFRalpha and phosphorylated eIF-2alpha were assessed via Western blotting.
RNA and protein synthesis inhibition experiments (actinomycin D, cycloheximide) were performed.

Main Results:

HDAC inhibitor treatment enhanced the decrease in FIP1L1-PDGFRalpha protein levels when RNA synthesis was inhibited.
Protein synthesis inhibition did not alter FIP1L1-PDGFRalpha protein levels.
Continuous eIF-2alpha phosphorylation was observed for up to 8 days post-treatment.

Conclusions:

The reduction in FIP1L1-PDGFRalpha protein by HDAC inhibition is likely due to decreased translation of FIP1L1-PDGFRA mRNA.
This suggests a post-transcriptional regulatory mechanism impacting oncogenic protein levels.