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
酶
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]
日期:2014-11-06
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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