Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.8748
Title: XAF1 promotes neuroblastoma tumor suppression and is required for KIF1B?-mediated apoptosis
Authors: Choo, Z 
Koh, R.Y.L
Wallis, K
Koh, T.J.W
Kuick, C.H
Sobrado, V
Kenchappa, R.S
Loh, A.H.P 
Soh, S.Y 
Schlisio, S
Chang, K.T.E 
Chen, Z.X 
Keywords: caspase 3
cell protein
kinesin
protein KIF1B beta
short hairpin RNA
unclassified drug
XIAP associated factor 1
F box protein
KIF1B protein, human
Kif1b protein, mouse
kinesin
signal peptide
tumor marker
tumor protein
tumor suppressor protein
XAF1 protein, human
XAF1 protein, mouse
animal cell
animal experiment
animal model
animal tissue
apoptosis
Article
bioinformatics
cancer inhibition
cancer prognosis
cancer survival
cell viability
controlled study
disease status
female
gene silencing
general aspects of disease
genetic transfection
human
human cell
human tissue
in vitro study
in vivo study
knockout mouse
major clinical study
molecular dynamics
mouse
neuroblastoma
neuroprotection
nonhuman
overall survival
protein analysis
protein cleavage
protein expression
protein function
survival rate
survival time
tumor growth
tumor volume
animal
apoptosis
gene expression regulation
Kaplan Meier method
metabolism
mortality
neuroblastoma
pathology
physiology
prognosis
tumor cell line
xenograft
Animals
Apoptosis
Biomarkers, Tumor
Cell Line, Tumor
F-Box Proteins
Gene Expression Regulation, Neoplastic
Heterografts
Humans
Intracellular Signaling Peptides and Proteins
Kaplan-Meier Estimate
Kinesin
Mice
Mice, Knockout
Neoplasm Proteins
Neuroblastoma
Prognosis
Tumor Suppressor Proteins
Issue Date: 2016
Citation: Choo, Z, Koh, R.Y.L, Wallis, K, Koh, T.J.W, Kuick, C.H, Sobrado, V, Kenchappa, R.S, Loh, A.H.P, Soh, S.Y, Schlisio, S, Chang, K.T.E, Chen, Z.X (2016). XAF1 promotes neuroblastoma tumor suppression and is required for KIF1B?-mediated apoptosis. Oncotarget 7 (23) : 34229-34239. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.8748
Abstract: Neuroblastoma is an aggressive, relapse-prone childhood tumor of the sympathetic nervous system. Current treatment modalities do not fully exploit the genetic basis between the different molecular subtypes and little is known about the targets discovered in recent mutational and genetic studies. Neuroblastomas with poor prognosis are often characterized by 1p36 deletion, containing the kinesin gene KIF1B. Its beta isoform, KIF1B?, is required for NGF withdrawal-dependent apoptosis, mediated by the induction of XIAP-associated Factor 1 (XAF1). Here, we showed that XAF1 low expression correlates with poor survival and disease status. KIF1B? deletion results in loss of XAF1 expression, suggesting that XAF1 is indeed a downstream target of KIF1B?. XAF1 silencing protects from NGF withdrawal and from KIF1B?-mediated apoptosis. Overexpression of XAF1 impairs tumor progression whereas knockdown of XAF1 promotes tumor growth, suggesting that XAF1 may be a candidate tumor suppressor in neuroblastoma and its associated pathway may be important for developing future interventions.
Source Title: Oncotarget
URI: https://scholarbank.nus.edu.sg/handle/10635/173827
ISSN: 19492553
DOI: 10.18632/oncotarget.8748
Appears in Collections:Staff Publications
Elements

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_18632_oncotarget_8748.pdf7.5 MBAdobe PDF

OPEN

NoneView/Download

SCOPUSTM   
Citations

9
checked on Dec 1, 2022

Page view(s)

175
checked on Dec 1, 2022

Download(s)

2
checked on Dec 1, 2022

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.