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Title 

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

Authors 

H J YongJ S ParkA L JeongS HanS LeeH I KaB SumiyasurenH J JooS J SoJ Y ParkD Y YoonJ S LimM S LeeHee Gu LeeY Yang

Publisher 

Impact Journals

Issue Date 

2017

Citation 

Oncotarget

Keywords 

ApoptosisHypoxiaInterleukin-32Protein kinase CVon 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 PKCd-induced apoptosis

ISSN 

1949-2553

Link 

http://dx.doi.org/10.18632/oncotarget.19311

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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