ScholarWorks@숙명여자대학교

초록

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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