Von Hippel-Lindau regulates interleukin-32 beta stability in ovarian cancer cellsopen access
- Authors
- Yong, Hyo Jeong; Park, Jeong Su; Jeong, Ae Lee; Han, Sora; Lee, Sunyi; Ka, Hye In; Sumiyasuren, Buyanravjkh; Joo, Hyun Jeong; So, Su Jeong; Park, Ji Young; Yoon, Do-Young; Lim, Jong-Seok; Lee, Myeong-Seok; Lee, Hee Gu; Yang, Young
- Issue Date
- Sep-2017
- Publisher
- IMPACT JOURNALS LLC
- Keywords
- interleukin-32; von Hippel-Lindau; protein kinase C; hypoxia; apoptosis
- Citation
- ONCOTARGET, v.8, no.41, pp 69833 - 69846
- Pages
- 14
- Journal Title
- ONCOTARGET
- Volume
- 8
- Number
- 41
- Start Page
- 69833
- End Page
- 69846
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8151
- DOI
- 10.18632/oncotarget.19311
- ISSN
- 1949-2553
1949-2553
- Abstract
- Hypoxia-induced interleukin-32 beta (IL-32 beta) shifts the metabolic program to the enhanced glycolytic pathway. In the present study, the underlying mechanism by which hypoxia-induced IL-32 beta stability is regulated was investigated in ovarian cancer cells. IL-32 beta expression increased under hypoxic conditions in ovarian cancer cells as it did in breast cancer cells. The amount of IL-32 beta was regulated by post-translational control rather than by transcriptional activation. Under normoxic conditions, IL-32 beta 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-32 beta and VHL, leading to the accumulation of the cytokine. The fact that IL-32 beta is regulated by the energy-consuming ubiquitination system implies that it plays an important role in oxidative stress. We found that IL-32 beta reduced protein kinase C delta (PKC delta)-induced apoptosis under oxidative stress. This implies that the hypoxia- and ROS-stabilized IL-32 beta contributes to sustain survival against PKC delta-induced apoptosis.
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