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Von Hippel-Lindau regulates interleukin-32β stability in ovarian cancer cells

Authors
 Hyo Jeong Yong  ;  Jeong Su Park  ;  Ae Lee Jeong  ;  Sora Han  ;  Sunyi Lee  ;  Hye In Ka  ;  Buyanravjkh Sumiyasuren  ;  Hyun Jeong Joo  ;  Su Jeong So  ;  Ji Young Park  ;  Do-Young Yoon  ;  Jong-Seok Lim  ;  Myeong-Seok Lee  ;  Hee Gu Lee  ;  Young Yang 
Citation
 ONCOTARGET, Vol.8(41) : 69833-69846, 2017-09 
Journal Title
ONCOTARGET
Issue Date
2017-09
Keywords
apoptosis ; hypoxia ; interleukin-32 ; protein kinase C ; von Hippel-Lindau
Abstract
Hypoxia-induced interleukin-32β (IL-32β) shifts the metabolic program to the enhanced glycolytic pathway. In the present study, the underlying mechanism by which hypoxia-induced IL-32β stability is regulated was investigated in ovarian cancer cells. IL-32β expression increased under hypoxic conditions in ovarian cancer cells as it did in breast cancer cells. The amount of IL-32β was regulated by post-translational control rather than by transcriptional activation. Under normoxic conditions, IL-32β was continuously eliminated through ubiquitin-dependent degradation by the von-Hippel Lindau (VHL) E3 ligase complex. Oxygen deficiency or reactive oxygen species (ROS) disrupted the interaction between IL-32β and VHL, leading to the accumulation of the cytokine. The fact that IL-32β is regulated by the energy-consuming ubiquitination system implies that it plays an important role in oxidative stress. We found that IL-32β reduced protein kinase Cδ (PKCδ)-induced apoptosis under oxidative stress. This implies that the hypoxia- and ROS-stabilized IL-32β contributes to sustain survival against PKCδ-induced apoptosis.
Files in This Item:
T992017117.pdf Download
DOI
10.18632/oncotarget.19311
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Park, Jeong Su(박정수) ORCID logo https://orcid.org/0000-0003-4551-4294
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/195851
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