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本文引用的文献

1
K-ras(G12V) transformation leads to mitochondrial dysfunction and a metabolic switch from oxidative phosphorylation to glycolysis.K-ras(G12V) 转化导致线粒体功能障碍和代谢从氧化磷酸化向糖酵解的转变。
Cell Res. 2012 Feb;22(2):399-412. doi: 10.1038/cr.2011.145. Epub 2011 Aug 30.
2
Anticancer drugs targeting the mitochondrial electron transport chain.靶向线粒体电子传递链的抗癌药物。
Antioxid Redox Signal. 2011 Dec 15;15(12):2951-74. doi: 10.1089/ars.2011.3990. Epub 2011 Sep 1.
3
Hallmarks of cancer: the next generation.癌症的特征:下一代。
Cell. 2011 Mar 4;144(5):646-74. doi: 10.1016/j.cell.2011.02.013.
4
Global cancer statistics.全球癌症统计数据。
CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90. doi: 10.3322/caac.20107. Epub 2011 Feb 4.
5
Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity.线粒体代谢和 ROS 生成对于 Kras 介导的肿瘤发生是必不可少的。
Proc Natl Acad Sci U S A. 2010 May 11;107(19):8788-93. doi: 10.1073/pnas.1003428107. Epub 2010 Apr 26.
6
The causes of cancer revisited: "mitochondrial malignancy" and ROS-induced oncogenic transformation - why mitochondria are targets for cancer therapy.癌症成因再探:“线粒体恶性肿瘤”与 ROS 诱导的致癌转化——线粒体为何成为癌症治疗靶点。
Mol Aspects Med. 2010 Apr;31(2):145-70. doi: 10.1016/j.mam.2010.02.008. Epub 2010 Mar 2.
7
Glucose deprivation contributes to the development of KRAS pathway mutations in tumor cells.葡萄糖剥夺促进肿瘤细胞中KRAS信号通路突变的发生。
Science. 2009 Sep 18;325(5947):1555-9. doi: 10.1126/science.1174229. Epub 2009 Aug 6.
8
Mitochondrial STAT3 supports Ras-dependent oncogenic transformation.线粒体 STAT3 支持 Ras 依赖性致癌转化。
Science. 2009 Jun 26;324(5935):1713-6. doi: 10.1126/science.1171721.
9
Understanding the Warburg effect: the metabolic requirements of cell proliferation.理解瓦伯格效应:细胞增殖的代谢需求。
Science. 2009 May 22;324(5930):1029-33. doi: 10.1126/science.1160809.
10
Alpha-tocopheryl succinate induces apoptosis by targeting ubiquinone-binding sites in mitochondrial respiratory complex II.琥珀酸生育酚通过靶向线粒体呼吸复合物II中的泛醌结合位点诱导细胞凋亡。
Oncogene. 2008 Jul 17;27(31):4324-35. doi: 10.1038/onc.2008.69. Epub 2008 Mar 31.

K-Ras 与线粒体:危险的联姻。

K-Ras and mitochondria: dangerous liaisons.

机构信息

Apoptosis Research Group, School of Medical Science, Griffith University Gold Coast Campus, Southport, 4222 Qld, Australia.

出版信息

Cell Res. 2012 Feb;22(2):285-7. doi: 10.1038/cr.2011.160. Epub 2011 Sep 27.

DOI:10.1038/cr.2011.160
PMID:21946499
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3271806/
Abstract

It is well documented that the oncogene efficiently transforms non-malignant cells, and there is some evidence for the role of mitochondria in this process. Now Peng Huang and colleagues show that K-Ras induction results early on in mitochondria assuming the phenotype consistent with the so-called Warburg effect, i.e., increased glycolysis and attenuated oxidative phosphorylation. Thus the K-Ras protein capable of swift induction of phenotypic changes typical of cancer cells, yet these changes are reversible, and for cells to irreversibly reach their full malignant potential a much longer K-Ras expression is required, implicating mitochondria in the longer-term effects of the oncogene.

摘要

有大量文献记载表明癌基因能够有效地转化非恶性细胞,并且有一些证据表明线粒体在这个过程中起作用。现在,Peng Huang 和他的同事们表明,K-Ras 的诱导导致线粒体早期表现出与所谓的Warburg 效应一致的表型,即增加糖酵解和减弱氧化磷酸化。因此,K-Ras 蛋白能够迅速诱导类似于癌细胞的表型变化,但这些变化是可逆的,而细胞要不可逆地达到其完全恶性的潜力,则需要更长时间的 K-Ras 表达,这表明线粒体参与了癌基因的长期效应。