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PCI-24781 induces caspase and reactive oxygen species-dependent apoptosis through NF-κB mechanisms and is synergistic with bortezomib in lymphoma cells
Savita Bhalla; Sriram Balasubramanian; Kevin David; Mint Sirisawad; Joseph Buggy; Lauren Mauro; Sheila Prachand; Richard Miller; Leo I. Gordon; Andrew M. Evens (Profiled Authors: Savita Bhalla; Leo I Gordon)
Clinical Cancer Research. 2009;15(10):3354-3365.Abstract
Purpose: We investigated the cytotoxicity and mechanisms of cell death of the broad-spectrum histone deacetylase (HDAC) inhibitor PCI-24781, alone and combined with bortezomib in Hodgkin lymphoma and non-Hodgkin lymphoma cell lines and primary lymphoproliferative (CLL/SLL) cells. Experimental Design: Apoptosis, mitochondrial membrane potential, cell cycle analysis, and reactive oxygen species (ROS) were measured by flow cytometry, whereas caspase activation was determined by Western blot. Nuclear factor κB (NF-κB)-related mRNAs were quantified by reverse transcription-PCR, NF-κB-related proteins by Western blotting, and NF-κB DNA-binding activity by electromobility shift assay. Finally, gene expression profiling was analyzed. Results: PCI-24781 induced concentration-dependent apoptosis that was associated with prominent G
PMID: 19417023 PMCID: PMC2704489
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