缺氧诱导因子 1：癌症代谢的上下游。
HIF-1: upstream and downstream of cancer metabolism.
机构信息
Vascular Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Broadway Research Building, Suite 671, 733 North Broadway, Baltimore, MD 21205, United States.
出版信息
Curr Opin Genet Dev. 2010 Feb;20(1):51-6. doi: 10.1016/j.gde.2009.10.009. Epub 2009 Nov 26.
Abstract
Hypoxia-inducible factor 1 (HIF-1) plays a key role in the reprogramming of cancer metabolism by activating transcription of genes encoding glucose transporters and glycolytic enzymes, which take up glucose and convert it to lactate; pyruvate dehydrogenase kinase 1, which shunts pyruvate away from the mitochondria; and BNIP3, which triggers selective mitochondrial autophagy. The shift from oxidative to glycolytic metabolism allows maintenance of redox homeostasis and cell survival under conditions of prolonged hypoxia. Many metabolic abnormalities in cancer cells increase HIF-1 activity. As a result, a feed-forward mechanism can be activated that drives HIF-1 activation and may promote tumor progression.
摘要
缺氧诱导因子 1（HIF-1）通过激活葡萄糖转运蛋白和糖酵解酶的基因转录，在癌症代谢的重编程中发挥关键作用，这些基因编码的蛋白摄取葡萄糖并将其转化为乳酸；丙酮酸脱氢酶激酶 1，将丙酮酸从线粒体分流；以及 BNIP3，触发选择性线粒体自噬。从氧化代谢到糖酵解代谢的转变允许在长期缺氧的情况下维持氧化还原平衡和细胞存活。癌细胞中的许多代谢异常增加了 HIF-1 的活性。因此，可以激活正反馈机制，从而激活 HIF-1 并可能促进肿瘤进展。
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