SIRT3 通过调节 ROS 和 HIF 来控制癌症代谢重编程。
SIRT3 controls cancer metabolic reprogramming by regulating ROS and HIF.
机构信息
Department of Pediatrics, Northwestern University Feinberg School of Medicine, 310 E. Superior St. Searle Bldg. 4-685, Chicago, IL 60611, USA.
出版信息
Cancer Cell. 2011 Mar 8;19(3):299-300. doi: 10.1016/j.ccr.2011.03.001.
Abstract
In this issue of Cancer Cell, Finley and coworkers report that the genetic loss of the deacetylase SIRT3 leads to metabolic reprogramming toward glycolysis. This shift is mediated by an increase in cellular reactive oxygen species (ROS) generation that amplifies HIF-α stabilization and HIF-dependent gene expression, thereby driving the tumor phenotype.
摘要
在本期《癌细胞》杂志中，Finley 及其同事报告称，去乙酰化酶 SIRT3 的遗传缺失会导致代谢向糖酵解重新编程。这种转变是由细胞内活性氧（ROS）生成的增加介导的，它放大了 HIF-α 的稳定和 HIF 依赖性基因表达，从而驱动肿瘤表型。
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本文引用的文献
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SIRT3 opposes reprogramming of cancer cell metabolism through HIF1α destabilization.SIRT3 通过使 HIF1α 不稳定来抵制癌细胞代谢的重编程。
Cancer Cell. 2011 Mar 8;19(3):416-28. doi: 10.1016/j.ccr.2011.02.014.
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