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FOXO3 induces ubiquitylation of AKT through MUL1 regulation

Authors
 Sun-Yong Kim  ;  Hyo Jeong Kim  ;  Hyung Kwon Byeon  ;  Dae Ho Kim  ;  Chul-Ho Kim 
Citation
 ONCOTARGET, Vol.8(66) : 110474-110489, 2017-11 
Journal Title
ONCOTARGET
Issue Date
2017-11
Keywords
AKT ; FOXO3 ; MUL1/MULAN/GIDE ; cisplatin ; ubiquitylation
Abstract
AKT (also known as protein kinase B, PKB) plays an important role in cell survival or tumor progression. For these reasons, AKT is an emerging target for cancer therapeutics. Previously our studies showed that mitochondrial E3 ubiquitin protein ligase 1 (MUL1, also known as MULAN/GIDE/MAPL) is suppressed in head and neck cancer (HNC) and acts as negative regulator against AKT. However, the MUL1 regulatory mechanisms remain largely unknown. Here we report that cisplatin (CDDP) induces thyroid cancer cell death through MUL1-AKT axis. Specifically, CDDP-induced MUL1 leads to ubiquitylation of active form of AKT. We also observed that the role of forkhead box O3 (FOXO3) is pivotal in CDDP-induced MUL1 regulation. FOXO3 knock-downed cells show resistance against CDDP-mediated MUL1-AKT axis. CDDP-mediated intracellular ROS increment plays an important role in FOXO3-MUL1-AKT signal pathway. The data provide compelling evidence to support the idea that the regulation of FOXO3-MUL1-AKT axis can be a novel strategy for the treatment of HNC with CDDP.
Files in This Item:
T999201735.pdf Download
DOI
10.18632/oncotarget.22793
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
Yonsei Authors
Byeon, Hyung Kwon(변형권)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/195845
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