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Updated: Jul 19, 2026

Assays for Validating Histone Acetyltransferase Inhibitors
Published on: August 6, 2020
Histone deacetylase inhibitors induce cell death in supratentorial primitive neuroectodermal tumor cells
K Saravana Kumar1, Jürgen Sonnemann, James F Beck
1Research Center of Pharmacology and Experimental Therapeutics, Ernst Moritz Arndt University of Greifswald, D-17487 Greifswald, Germany.
Abstract:
Histone deacetylase inhibitors (HDIs) are a promising new class of antineoplastic agents with the capacity to induce differentiation and/or apoptosis of cancer cells. The objective of this study was to evaluate the activity of HDIs against supratentorial primitive neuroectodermal tumor (sPNET) cells. We show that the HDIs, suberoylanilide hydroxamic acid, sodium butyrate, and trichostatin A, induced cell death, and activated caspase-3 and -9 in a sPNET cell line, PFSK. The poly-caspase inhibitor z-VAD-fmk partially prevented the action of HDIs, as judged by determining the mitochondrial membrane potential and by quantifying internucleosomal DNA fragmentation. In conclusion, the HDIs explored possess potent activity against sPNET cells, suggesting that HDIs may be effective in the treatment of sPNET.
Insights
Histone deacetylase inhibitors (HDIs) show potent anticancer activity by inducing cell death in supratentorial primitive neuroectodermal tumor (sPNET) cells. These findings suggest HDIs may be effective for treating sPNET.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Histone deacetylase inhibitors (HDIs) are emerging antineoplastic agents.
- HDIs demonstrate potential in inducing cancer cell differentiation and apoptosis.
Purpose of the Study:
- To evaluate the efficacy of HDIs against supratentorial primitive neuroectodermal tumor (sPNET) cells.
- To investigate the mechanisms of HDI-induced cell death in sPNET.
Main Methods:
- Utilized a sPNET cell line (PFSK).
- Administered HDIs: suberoylanilide hydroxamic acid, sodium butyrate, and trichostatin A.
- Assessed cell death, caspase-3 and -9 activation, mitochondrial membrane potential, and DNA fragmentation.
- Employed a poly-caspase inhibitor (z-VAD-fmk) to elucidate apoptotic pathways.
Main Results:
- HDIs effectively induced cell death in the sPNET cell line.
- Activation of caspase-3 and -9 was observed following HDI treatment.
- Partial inhibition of HDI effects was noted with z-VAD-fmk, impacting mitochondrial potential and DNA fragmentation.
Conclusions:
- The studied HDIs exhibit significant cytotoxic effects on sPNET cells.
- HDIs represent a promising therapeutic strategy for sPNET treatment.
- Further investigation into HDIs for sPNET therapy is warranted.
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