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Cancer: when antioxidants are bad.

作者信息

Perera Rushika M, Bardeesy Nabeel

机构信息

Massachusetts General Hospital, Cancer Center, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02114, USA.

出版信息

Nature. 2011 Jul 6;475(7354):43-4. doi: 10.1038/475043a.

DOI:10.1038/475043a
PMID:21734699
Abstract
摘要

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本文引用的文献

1
Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis.癌基因诱导的 Nrf2 转录促进 ROS 解毒和肿瘤发生。
Nature. 2011 Jul 6;475(7354):106-9. doi: 10.1038/nature10189.
2
Pancreatic cancers require autophagy for tumor growth.胰腺癌的生长需要自噬作用。
Genes Dev. 2011 Apr 1;25(7):717-29. doi: 10.1101/gad.2016111. Epub 2011 Mar 15.
3
Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?通过活性氧介导的机制靶向癌细胞：一种激进的治疗方法？
BDH2 通过促进胃癌中 Nrf2 的泛素化来触发 ROS 诱导的细胞死亡和自噬。
J Exp Clin Cancer Res. 2020 Jun 30;39(1):123. doi: 10.1186/s13046-020-01620-z.
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Loss-of-function mutations in KEAP1 drive lung cancer progression via KEAP1/NRF2 pathway activation.KEAP1 失活突变通过 KEAP1/NRF2 通路激活驱动肺癌进展。
Cell Commun Signal. 2020 Jun 23;18(1):98. doi: 10.1186/s12964-020-00568-z.
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MicroRNA-421 confers paclitaxel resistance by binding to the KEAP1 3'UTR and predicts poor survival in non-small cell lung cancer.miRNA-421 通过与 KEAP1 3'UTR 结合赋予紫杉醇耐药性，并预测非小细胞肺癌患者的生存不良。
Cell Death Dis. 2019 Oct 28;10(11):821. doi: 10.1038/s41419-019-2031-1.
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Contribution of Nrf2 Modulation to the Mechanism of Action of Analgesic and Anti-inflammatory Drugs in Pre-clinical and Clinical Stages.Nrf2调节在临床前和临床阶段对镇痛和抗炎药物作用机制的贡献。
Front Pharmacol. 2019 Jan 11;9:1536. doi: 10.3389/fphar.2018.01536. eCollection 2018.
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KRas, ROS and the initiation of pancreatic cancer.KRas、活性氧和胰腺癌的起始
Small GTPases. 2017 Jan 2;8(1):38-42. doi: 10.1080/21541248.2016.1192714. Epub 2016 May 24.
8
Mutant KRas-Induced Mitochondrial Oxidative Stress in Acinar Cells Upregulates EGFR Signaling to Drive Formation of Pancreatic Precancerous Lesions.突变型KRas诱导的腺泡细胞线粒体氧化应激上调EGFR信号传导，以驱动胰腺癌前病变的形成。
Cell Rep. 2016 Mar 15;14(10):2325-36. doi: 10.1016/j.celrep.2016.02.029. Epub 2016 Mar 3.
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Antioxidant therapy for treatment of inflammatory bowel disease: Does it work?抗氧化疗法治疗炎症性肠病：有效吗？
Redox Biol. 2015 Dec;6:617-639. doi: 10.1016/j.redox.2015.10.006. Epub 2015 Oct 23.
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In Vitro and In Vivo Studies of Non-Platinum-Based Halogenated Compounds as Potent Antitumor Agents for Natural Targeted Chemotherapy of Cancers.体外和体内研究非铂类卤代化合物作为癌症天然靶向化疗的有效抗肿瘤药物。
EBioMedicine. 2015 Apr 20;2(6):544-53. doi: 10.1016/j.ebiom.2015.04.011. eCollection 2015 Jun.
Nat Rev Drug Discov. 2009 Jul;8(7):579-91. doi: 10.1038/nrd2803. Epub 2009 May 29.
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NRF2 and KEAP1 mutations: permanent activation of an adaptive response in cancer.NRF2和KEAP1突变：癌症中适应性反应的永久激活。
Trends Biochem Sci. 2009 Apr;34(4):176-88. doi: 10.1016/j.tibs.2008.12.008. Epub 2009 Mar 25.
5
c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism.c-Myc对miR-23a/b的抑制作用增强了线粒体谷氨酰胺酶的表达及谷氨酰胺代谢。
Nature. 2009 Apr 9;458(7239):762-5. doi: 10.1038/nature07823. Epub 2009 Feb 15.
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HIF-dependent antitumorigenic effect of antioxidants in vivo.体内抗氧化剂的低氧诱导因子依赖性抗肿瘤作用。
Cancer Cell. 2007 Sep;12(3):230-8. doi: 10.1016/j.ccr.2007.08.004.
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Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway.细胞通过Keap1-Nrf2-ARE途径对环境应激的存活反应。
Annu Rev Pharmacol Toxicol. 2007;47:89-116. doi: 10.1146/annurev.pharmtox.46.120604.141046.
8
The antioxidant function of the p53 tumor suppressor.p53肿瘤抑制因子的抗氧化功能。
Nat Med. 2005 Dec;11(12):1306-13. doi: 10.1038/nm1320. Epub 2005 Nov 13.
9
c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability.c-Myc可诱导DNA损伤、增加活性氧并削弱p53功能：一种癌基因诱导的基因不稳定机制。
Mol Cell. 2002 May;9(5):1031-44. doi: 10.1016/s1097-2765(02)00520-8.
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Mitogenic signaling mediated by oxidants in Ras-transformed fibroblasts.Ras 转化的成纤维细胞中由氧化剂介导的促有丝分裂信号传导。
Science. 1997 Mar 14;275(5306):1649-52. doi: 10.1126/science.275.5306.1649.