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Title: RuvBL2 Is Involved in Histone Deacetylase Inhibitor PCI-24781-Induced Cell Death in SK-N-DZ Neuroblastoma Cells
Authors: Zhan Q.
Tsai S.
Lu Y. 
Wang C.
Kwan Y.
Ngai S.
Keywords: abexinostat
caspase 3
death receptor 4
protein hHR23a
protein p21
protein p53
protein PDCD6IP
protein RuvBL2
protein trap1
unclassified drug
amino acid sequence
antineoplastic activity
cancer cell culture
cell cycle arrest
cell cycle G2 phase
cell proliferation
cell viability
concentration response
controlled study
drug dose increase
gene silencing
HS 68 cell ine
human cell
matrix assisted laser desorption ionization time of flight mass spectrometry
neuroblastoma cell
protein expression
signal transduction
transcription regulation
tumor growth
Western blotting
Blotting, Western
Carrier Proteins
Cell Line, Tumor
DNA Helicases
G2 Phase Cell Cycle Checkpoints
Histone Deacetylase Inhibitors
Hydroxamic Acids
Models, Biological
Neoplasm Proteins
Reproducibility of Results
Signal Transduction
Issue Date: 2013
Citation: Zhan Q., Tsai S., Lu Y., Wang C., Kwan Y., Ngai S. (2013). RuvBL2 Is Involved in Histone Deacetylase Inhibitor PCI-24781-Induced Cell Death in SK-N-DZ Neuroblastoma Cells. PLoS ONE 8 (8) : e71663. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Neuroblastoma is the second most common solid tumor diagnosed during infancy. The survival rate among children with high-risk neuroblastoma is less than 40%, highlighting the urgent needs for new treatment strategies. PCI-24781 is a novel hydroxamic acid-based histone deacetylase (HDAC) inhibitor that has high efficacy and safety for cancer treatment. However, the underlying mechanisms of PCI-24781 are not clearly elucidated in neuroblastoma cells. In the present study, we demonstrated that PCI-24781 treatment significantly inhibited tumor growth at very low doses in neuroblastoma cells SK-N-DZ, not in normal cell line HS-68. However, PCI-24781 caused the accumulation of acetylated histone H3 both in SK-N-DZ and HS-68 cell line. Treatment of SK-N-DZ with PCI-24781 also induced cell cycle arrest in G2/M phase and activated apoptosis signaling pathways via the up-regulation of DR4, p21, p53 and caspase 3. Further proteomic analysis revealed differential protein expression profiles between non-treated and PCI-24781 treated SK-N-DZ cells. Totally 42 differentially expressed proteins were identified by MALDI-TOF MS system. Western blotting confirmed the expression level of five candidate proteins including prohibitin, hHR23a, RuvBL2, TRAP1 and PDCD6IP. Selective knockdown of RuvBL2 rescued cells from PCI-24781-induced cell death, implying that RuvBL2 might play an important role in anti-tumor activity of PCI-24781 in SK-N-DZ cells. The present results provide a new insight into the potential mechanism of PCI-24781 in SK-N-DZ cell line. © 2013 Zhan et al.
Source Title: PLoS ONE
ISSN: 19326203
DOI: 10.1371/journal.pone.0071663
Rights: Attribution 4.0 International
Appears in Collections:Staff Publications

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