Hypoxia-induced IL-32β increases glycolysis in breast cancer cells

糖酵解 缺氧(环境) 氧化磷酸化 厌氧糖酵解 生物 线粒体 乳酸脱氢酶 线粒体生物发生 线粒体ROS NADPH氧化酶 细胞生物学 化学 活性氧 生物化学 新陈代谢 氧气 有机化学
作者
Jeong Su Park,Sunyi Lee,Ae Lee Jeong,Sora Han,Hye In Ka,Jong‐Seok Lim,Myung Sok Lee,Do‐Young Yoon,Jeong‐Hyung Lee,Young Yang
出处
期刊:Cancer Letters [Elsevier]
卷期号:356 (2): 800-808 被引量:33
标识
DOI:10.1016/j.canlet.2014.10.030
摘要

IL-32β is highly expressed and increases the migration and invasion of gastric, lung, and breast cancer cells. Since IL-32 enhances VEGF production under hypoxic conditions, whether IL-32β is regulated by hypoxia was examined. Hypoxic conditions and a mimetic chemical CoCl2 enhanced IL-32β production. When cells were treated with various inhibitors of ROS generation to prevent hypoxia-induced ROS function, IL-32β production was suppressed by both NADPH oxidase and mitochondrial ROS inhibitors. IL-32β translocated to the mitochondria under hypoxic conditions, where it was associated with mitochondrial biogenesis. Thus, whether hypoxia-induced IL-32β is associated with oxidative phosphorylation (OXPHOS) or glycolysis was examined. Glycolysis under aerobic and anaerobic conditions is impaired in IL-32β-depleted cells, and the hypoxia-induced IL-32β increased glycolysis through activation of lactate dehydrogenase. Src is also known to increase lactate dehydrogenase activity, and the hypoxia-induced IL-32β was found to stimulate Src activation by inhibiting the dephosphorylation of Src. These findings revealed that a hypoxia-ROS-IL-32β-Src-glycolysis pathway is associated with the regulation of cancer cell metabolism.

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