Please use this identifier to cite or link to this item:
https://doi.org/10.1371/journal.pone.0071663
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 prohibitin protein hHR23a protein p21 protein p53 protein PDCD6IP protein RuvBL2 protein trap1 unclassified drug amino acid sequence antineoplastic activity apoptosis article 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 human cell matrix assisted laser desorption ionization time of flight mass spectrometry neuroblastoma cell protein expression proteomics signal transduction transcription regulation tumor growth upregulation Western blotting Acetylation Apoptosis Benzofurans Blotting, Western Carrier Proteins Cell Line, Tumor DNA Helicases G2 Phase Cell Cycle Checkpoints Histone Deacetylase Inhibitors Histones Humans Hydroxamic Acids Male Mitosis Models, Biological Neoplasm Proteins Neuroblastoma Proteomics 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. https://doi.org/10.1371/journal.pone.0071663 | 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 | URI: | https://scholarbank.nus.edu.sg/handle/10635/161277 | ISSN: | 19326203 | DOI: | 10.1371/journal.pone.0071663 | Rights: | Attribution 4.0 International |
Appears in Collections: | Staff Publications Elements |
Show full item record
Files in This Item:
File | Description | Size | Format | Access Settings | Version | |
---|---|---|---|---|---|---|
10_1371_journal_pone_0071663.pdf | 1.99 MB | Adobe PDF | OPEN | None | View/Download |
This item is licensed under a Creative Commons License