Preventing Dr. Jekyll from becoming Mr. Hyde: is manganese superoxide dismutase the key to prevent radiation-induced neoplastic transformation?
作者信息
Holley Aaron K, St Clair Daret K
机构信息
Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA.
出版信息
Cancer Biol Ther. 2009 Oct;8(20):1972-3. doi: 10.4161/cbt.8.20.9941. Epub 2009 Oct 27.
Abstract
摘要
相似文献
1
Preventing Dr. Jekyll from becoming Mr. Hyde: is manganese superoxide dismutase the key to prevent radiation-induced neoplastic transformation?防止杰基尔博士变成海德先生：锰超氧化物歧化酶是预防辐射诱导肿瘤转化的关键吗？
Cancer Biol Ther. 2009 Oct;8(20):1972-3. doi: 10.4161/cbt.8.20.9941. Epub 2009 Oct 27.
2
Mitochondrial ROS and radiation induced transformation in mouse embryonic fibroblasts.线粒体 ROS 与辐射诱导的小鼠胚胎成纤维细胞转化。
Cancer Biol Ther. 2009 Oct;8(20):1962-71. doi: 10.4161/cbt.8.20.9648. Epub 2009 Oct 29.
3
Increased manganese superoxide dismutase activity, protein, and mRNA levels and concurrent induction of tumor necrosis factor alpha in radiation-initiated Syrian hamster cells.
Mol Carcinog. 1996 Dec;17(4):175-80. doi: 10.1002/(SICI)1098-2744(199612)17:4<175::AID-MC1>3.0.CO;2-D.
4
Loss of C/EBPδ enhances IR-induced cell death by promoting oxidative stress and mitochondrial dysfunction.C/EBPδ的缺失通过促进氧化应激和线粒体功能障碍增强电离辐射诱导的细胞死亡。
Free Radic Biol Med. 2016 Oct;99:296-307. doi: 10.1016/j.freeradbiomed.2016.08.022. Epub 2016 Aug 20.
5
Decreased pulmonary radiation resistance of manganese superoxide dismutase (MnSOD)-deficient mice is corrected by human manganese superoxide dismutase-Plasmid/Liposome (SOD2-PL) intratracheal gene therapy.通过人锰超氧化物歧化酶-质粒/脂质体（SOD2-PL）气管内基因治疗可纠正锰超氧化物歧化酶（MnSOD）缺陷小鼠降低的肺辐射抗性。
Radiat Res. 2000 Oct;154(4):365-74. doi: 10.1667/0033-7587(2000)154[0365:dprrom]2.0.co;2.
6
Impact of intercellular induction of apoptosis on low-dose radiation carcinogenesis.细胞间凋亡诱导对低剂量辐射致癌作用的影响。
Radiat Prot Dosimetry. 2015 Sep;166(1-4):170-3. doi: 10.1093/rpd/ncv169. Epub 2015 Apr 21.
7
Suppression of radiation-induced neoplastic transformation by overexpression of mitochondrial superoxide dismutase.通过线粒体超氧化物歧化酶的过表达抑制辐射诱导的肿瘤转化。
Mol Carcinog. 1992;6(4):238-42. doi: 10.1002/mc.2940060404.
8
Mitochondrial oxidative stress causes chromosomal instability of mouse embryonic fibroblasts.线粒体氧化应激导致小鼠胚胎成纤维细胞的染色体不稳定。
Aging Cell. 2003 Oct;2(5):277-85. doi: 10.1046/j.1474-9728.2003.00062.x.
9
The role of superoxide dismutase and gene amplification in carcinogenesis.超氧化物歧化酶的作用及基因扩增在致癌过程中的作用。
J Theor Biol. 1984 Feb 7;106(3):403-22. doi: 10.1016/0022-5193(84)90038-9.
10
Differential responses of SOD1-deficient mouse embryonic fibroblasts to oxygen concentrations.SOD1 缺陷型小鼠胚胎成纤维细胞对氧浓度的差异反应。
Arch Biochem Biophys. 2013 Sep 1;537(1):5-11. doi: 10.1016/j.abb.2013.06.008. Epub 2013 Jun 27.
引用本文的文献
1
Radiation-Induced Oral Mucositis.放射性口腔黏膜炎
Front Oncol. 2017 May 22;7:89. doi: 10.3389/fonc.2017.00089. eCollection 2017.
2
Lack of p53 decreases basal oxidative stress levels in the brain through upregulation of thioredoxin-1, biliverdin reductase-A, manganese superoxide dismutase, and nuclear factor kappa-B.缺乏 p53 通过上调硫氧还蛋白-1、胆红素还原酶-A、锰超氧化物歧化酶和核因子 kappa-B 降低大脑中的基础氧化应激水平。
Antioxid Redox Signal. 2012 Jun 15;16(12):1407-20. doi: 10.1089/ars.2011.4124. Epub 2012 Feb 21.
本文引用的文献
1
Mitochondrial ROS and radiation induced transformation in mouse embryonic fibroblasts.线粒体 ROS 与辐射诱导的小鼠胚胎成纤维细胞转化。
Cancer Biol Ther. 2009 Oct;8(20):1962-71. doi: 10.4161/cbt.8.20.9648. Epub 2009 Oct 29.
2
Reduced mitochondrial SOD displays mortality characteristics reminiscent of natural aging.线粒体超氧化物歧化酶减少表现出类似于自然衰老的死亡特征。
Mech Ageing Dev. 2007 Nov-Dec;128(11-12):706-16. doi: 10.1016/j.mad.2007.10.013. Epub 2007 Nov 4.
3
Mitochondria: a hub of redox activities and cellular distress control.线粒体：氧化还原活动和细胞应激控制的中心
Mol Cell Biochem. 2007 Nov;305(1-2):235-53. doi: 10.1007/s11010-007-9520-8. Epub 2007 Jun 12.
4
Mechanism of the tumor suppressive effect of MnSOD overexpression.锰超氧化物歧化酶过表达的肿瘤抑制作用机制。
Biomed Pharmacother. 2005 May;59(4):143-8. doi: 10.1016/j.biopha.2005.03.006. Epub 2005 Mar 19.
5
A Sod2 null mutation confers severely reduced adult life span in Drosophila.超氧化物歧化酶2（Sod2）基因的无效突变会导致果蝇成年后的寿命大幅缩短。
Genetics. 2003 Dec;165(4):2295-9. doi: 10.1093/genetics/165.4.2295.
6
Life-long reduction in MnSOD activity results in increased DNA damage and higher incidence of cancer but does not accelerate aging.锰超氧化物歧化酶（MnSOD）活性的终身降低会导致DNA损伤增加和癌症发病率升高，但不会加速衰老。
Physiol Genomics. 2003 Dec 16;16(1):29-37. doi: 10.1152/physiolgenomics.00122.2003.
7
Manganese superoxide dismutase deficiency enhances cell turnover via tumor promoter-induced alterations in AP-1 and p53-mediated pathways in a skin cancer model.在皮肤癌模型中，锰超氧化物歧化酶缺乏通过肿瘤启动子诱导的AP-1和p53介导通路的改变增强细胞更新。
Oncogene. 2002 May 30;21(24):3836-46. doi: 10.1038/sj.onc.1205477.
8
9
Overexpression of manganese superoxide dismutase selectively modulates the activity of Jun-associated transcription factors in fibrosarcoma cells.
Cancer Res. 1997 Dec 1;57(23):5265-71.
10
Neurodegeneration, myocardial injury, and perinatal death in mitochondrial superoxide dismutase-deficient mice.
Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9782-7. doi: 10.1073/pnas.93.18.9782.
Zotero 插件