Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0071663
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dc.titleRuvBL2 Is Involved in Histone Deacetylase Inhibitor PCI-24781-Induced Cell Death in SK-N-DZ Neuroblastoma Cells
dc.contributor.authorZhan Q.
dc.contributor.authorTsai S.
dc.contributor.authorLu Y.
dc.contributor.authorWang C.
dc.contributor.authorKwan Y.
dc.contributor.authorNgai S.
dc.date.accessioned2019-11-04T04:03:15Z
dc.date.available2019-11-04T04:03:15Z
dc.date.issued2013
dc.identifier.citationZhan 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
dc.identifier.issn19326203
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/161277
dc.description.abstractNeuroblastoma 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.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20191101
dc.subjectabexinostat
dc.subjectcaspase 3
dc.subjectdeath receptor 4
dc.subjectprohibitin
dc.subjectprotein hHR23a
dc.subjectprotein p21
dc.subjectprotein p53
dc.subjectprotein PDCD6IP
dc.subjectprotein RuvBL2
dc.subjectprotein trap1
dc.subjectunclassified drug
dc.subjectamino acid sequence
dc.subjectantineoplastic activity
dc.subjectapoptosis
dc.subjectarticle
dc.subjectcancer cell culture
dc.subjectcell cycle arrest
dc.subjectcell cycle G2 phase
dc.subjectcell proliferation
dc.subjectcell viability
dc.subjectconcentration response
dc.subjectcontrolled study
dc.subjectdrug dose increase
dc.subjectgene silencing
dc.subjectHS 68 cell ine
dc.subjecthuman
dc.subjecthuman cell
dc.subjectmatrix assisted laser desorption ionization time of flight mass spectrometry
dc.subjectneuroblastoma cell
dc.subjectprotein expression
dc.subjectproteomics
dc.subjectsignal transduction
dc.subjecttranscription regulation
dc.subjecttumor growth
dc.subjectupregulation
dc.subjectWestern blotting
dc.subjectAcetylation
dc.subjectApoptosis
dc.subjectBenzofurans
dc.subjectBlotting, Western
dc.subjectCarrier Proteins
dc.subjectCell Line, Tumor
dc.subjectDNA Helicases
dc.subjectG2 Phase Cell Cycle Checkpoints
dc.subjectHistone Deacetylase Inhibitors
dc.subjectHistones
dc.subjectHumans
dc.subjectHydroxamic Acids
dc.subjectMale
dc.subjectMitosis
dc.subjectModels, Biological
dc.subjectNeoplasm Proteins
dc.subjectNeuroblastoma
dc.subjectProteomics
dc.subjectReproducibility of Results
dc.subjectSignal Transduction
dc.typeArticle
dc.contributor.departmentSAW SWEE HOCK SCHOOL OF PUBLIC HEALTH
dc.description.doi10.1371/journal.pone.0071663
dc.description.sourcetitlePLoS ONE
dc.description.volume8
dc.description.issue8
dc.description.pagee71663
dc.published.statePublished
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