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本文引用的文献

1
Sestrin2 integrates Akt and mTOR signaling to protect cells against energetic stress-induced death.Sestrin2 将 Akt 和 mTOR 信号整合在一起,以保护细胞免受能量应激诱导的死亡。
Cell Death Differ. 2013 Apr;20(4):611-9. doi: 10.1038/cdd.2012.157. Epub 2012 Dec 14.
2
AMPK regulates NADPH homeostasis to promote tumour cell survival during energy stress.AMPK 调节 NADPH 稳态以促进能量应激时肿瘤细胞的存活。
Nature. 2012 May 9;485(7400):661-5. doi: 10.1038/nature11066.
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The mTOR signalling pathway in human cancer.人类癌症中的mTOR信号通路。
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Suppression of FOXM1 sensitizes human cancer cells to cell death induced by DNA-damage.抑制 FOXM1 可使人类癌细胞对 DNA 损伤诱导的细胞死亡敏感。
PLoS One. 2012;7(2):e31761. doi: 10.1371/journal.pone.0031761. Epub 2012 Feb 29.
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Sestrin2 modulates AMPK subunit expression and its response to ionizing radiation in breast cancer cells.Sestrin2 调节乳腺癌细胞中 AMPK 亚基的表达及其对电离辐射的反应。
PLoS One. 2012;7(2):e32035. doi: 10.1371/journal.pone.0032035. Epub 2012 Feb 20.
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Exploiting cancer cell vulnerabilities to develop a combination therapy for ras-driven tumors.利用癌细胞的弱点开发针对 ras 驱动肿瘤的联合疗法。
Cancer Cell. 2011 Sep 13;20(3):400-13. doi: 10.1016/j.ccr.2011.08.014.
7
Oxidative stress, inflammation, and cancer: how are they linked?氧化应激、炎症与癌症:它们之间有何关联?
Free Radic Biol Med. 2010 Dec 1;49(11):1603-16. doi: 10.1016/j.freeradbiomed.2010.09.006. Epub 2010 Sep 16.
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FoxOs inhibit mTORC1 and activate Akt by inducing the expression of Sestrin3 and Rictor.FoxOs 通过诱导 Sestrin3 和 Rictor 的表达来抑制 mTORC1 并激活 Akt。
Dev Cell. 2010 Apr 20;18(4):592-604. doi: 10.1016/j.devcel.2010.03.008.
9
Sestrin as a feedback inhibitor of TOR that prevents age-related pathologies.Sesnrin 作为 TOR 的反馈抑制剂,可预防与年龄相关的病理。
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10
Glutathione S-transferases: an overview in cancer research.谷胱甘肽 S-转移酶:癌症研究概述。
Expert Opin Drug Metab Toxicol. 2010 Feb;6(2):153-70. doi: 10.1517/17425250903427980.

分子途径:癌细胞中活性氧物质的动态平衡及其对癌症治疗的影响。

Molecular pathways: reactive oxygen species homeostasis in cancer cells and implications for cancer therapy.

机构信息

Department of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60607,

出版信息

Clin Cancer Res. 2013 Aug 15;19(16):4309-14. doi: 10.1158/1078-0432.CCR-12-1424. Epub 2013 May 29.

DOI:10.1158/1078-0432.CCR-12-1424
PMID:23719265
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3933310/
Abstract

Reactive oxygen species (ROS) are important in regulating normal cellular processes, but deregulated ROS contribute to the development of various human diseases, including cancers. Cancer cells have increased ROS levels compared with normal cells, because of their accelerated metabolism. The high ROS levels in cancer cells, which distinguish them from normal cells, could be protumorigenic, but are also their Achilles' heel. The high ROS content in cancer cells renders them more susceptible to oxidative stress-induced cell death, and can be exploited for selective cancer therapy. In this review, we describe several potential therapeutic strategies that take advantage of ROS imbalance in cancer cells by further increasing oxidative stress, either alone or in combination with drugs that modulate certain signaling pathways.

摘要

活性氧(ROS)在调节正常细胞过程中很重要,但失调的 ROS 会导致各种人类疾病的发生,包括癌症。由于其代谢加速,癌细胞的 ROS 水平比正常细胞高。癌细胞中高 ROS 水平使它们与正常细胞区分开来,这可能是致癌的,但也是它们的致命弱点。癌细胞中高 ROS 含量使它们更容易受到氧化应激诱导的细胞死亡的影响,可以被利用来进行选择性癌症治疗。在这篇综述中,我们描述了几种潜在的治疗策略,通过进一步增加氧化应激,单独或与调节某些信号通路的药物联合使用,利用癌细胞中的 ROS 失衡。