Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41598-017-17192-6
Title: KIF1B? increases ROS to mediate apoptosis and reinforces its protein expression through O2 - In a positive feedback mechanism in neuroblastoma
Authors: Angelina, C 
Tan, I.S.Y
Choo, Z 
Lee, O.Z.J
Pervaiz, S 
Chen, Z.X 
Keywords: cation
diphenyliodonium salt
gliotoxin
KIF1B protein, human
kinesin
reactive oxygen metabolite
small interfering RNA
superoxide
antagonists and inhibitors
apoptosis
chemistry
drug effect
genetics
human
metabolism
neuroblastoma
pathology
protein synthesis
RNA interference
tumor cell line
upregulation
Apoptosis
Cell Line, Tumor
Gliotoxin
Humans
Kinesin
Neuroblastoma
Onium Compounds
Protein Biosynthesis
Reactive Oxygen Species
RNA Interference
RNA, Small Interfering
Superoxides
Up-Regulation
Issue Date: 2017
Citation: Angelina, C, Tan, I.S.Y, Choo, Z, Lee, O.Z.J, Pervaiz, S, Chen, Z.X (2017). KIF1B? increases ROS to mediate apoptosis and reinforces its protein expression through O2 - In a positive feedback mechanism in neuroblastoma. Scientific Reports 7 (1) : 17192. ScholarBank@NUS Repository. https://doi.org/10.1038/s41598-017-17192-6
Abstract: Relapse-prone, poor prognosis neuroblastoma is frequently characterized by deletion of chr1p36 where tumor suppressor gene KIF1B? resides. Interestingly, many 1p36-positive patients failed to express KIF1B? protein. Since altered cellular redox status has been reported to be involved in cell death and protein modification, we investigated the relationship between reactive oxygen species (ROS) and KIF1B?. Here, we showed that wild-type KIF1B? protein expression positively correlates with superoxide (O2 -) and total ROS levels in neuroblastoma cells, unlike apoptotic loss-of-function KIF1B? mutants. Overexpression of KIF1B? apoptotic domain variants increases total ROS and, specifically O2 -, whereas knockdown of endogenous KIF1B? decreases ROS and O2 -. Interestingly, O2 - increases KIF1B? protein expression, independent of the proteasomal degradation pathway. Scavenging O2 - or ROS decreases KIF1B? protein expression and subsequent apoptosis. Moreover, treatment with investigational redox compound Gliotoxin increases O2 -, KIF1B? protein expression, apoptosis and colony formation inhibition. Overall, our findings suggest that ROS and O2 - may be important downstream effectors of KIF1B?-mediated apoptosis. Subsequently, O2 - produced may increase KIF1B? protein expression in a positive feedback mechanism. Therefore, ROS and, specifically O2 -, may be critical regulators of KIF1B?-mediated apoptosis and its protein expression in neuroblastoma. © 2017 The Author(s).
Source Title: Scientific Reports
URI: https://scholarbank.nus.edu.sg/handle/10635/175088
ISSN: 20452322
DOI: 10.1038/s41598-017-17192-6
Appears in Collections:Elements
Staff Publications

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1038_s41598-017-17192-6.pdf2.99 MBAdobe PDF

OPEN

NoneView/Download

SCOPUSTM   
Citations

5
checked on Sep 21, 2022

Page view(s)

157
checked on Sep 22, 2022

Google ScholarTM

Check

Altmetric


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