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线粒体功能障碍与潜在的抗癌治疗。

Mitochondrial dysfunction and potential anticancer therapy.

机构信息

Oncology Program, Vall D'Hebron Research Institute, Barcelona, Spain.

Thomas Steitz Laboratory, Department of Molecular Biophysics & Biochemistry, Center for Structural Biology, Howard Hughes Medical Institute, Yale University, New Haven, Connecticut.

出版信息

Med Res Rev. 2017 Nov;37(6):1275-1298. doi: 10.1002/med.21459. Epub 2017 Jul 6.

DOI:10.1002/med.21459
PMID:28682452
Abstract

Mitochondrial dysfunction (MDF) has been identified as an important factor in various diseases ranging from neurological disorders, to diseases of the cardiovascular system and metabolic syndromes. MDF was also found in cancer as well as in cancer predisposition syndromes with defective DNA damage response (DDR) machinery. Moreover, a recent highlight arises from the detection of MDF in eukaryotic cells upon treatment with antibiotics. In this review, we focus on recent studies of MDF in pathological conditions with a particular emphasis on the effects of various classes of antibiotics on mitochondria. Special attention is given to the role of autophagy/mitophagy in MDF and repurposing antibiotics as anticancer drugs.

摘要

线粒体功能障碍(MDF)已被确定为各种疾病的重要因素,这些疾病范围从神经紊乱到心血管系统疾病和代谢综合征。MDF 也存在于癌症以及 DNA 损伤反应(DDR)机制有缺陷的癌症易感性综合征中。此外,最近的一个亮点是在使用抗生素治疗真核细胞时检测到 MDF。在这篇综述中,我们重点关注病理条件下 MDF 的最新研究,特别强调各种类别的抗生素对线粒体的影响。特别关注自噬/线粒体自噬在 MDF 中的作用以及将抗生素重新用作抗癌药物。

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Mitochondrial dysfunction and potential anticancer therapy.线粒体功能障碍与潜在的抗癌治疗。
Med Res Rev. 2017 Nov;37(6):1275-1298. doi: 10.1002/med.21459. Epub 2017 Jul 6.
2
Mitochondrial dysfunction in DDR-related cancer predisposition syndromes.DNA损伤修复(DDR)相关癌症易感综合征中的线粒体功能障碍
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Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition.通过抗生素诱导的线粒体功能障碍靶向癌细胞需要抑制自噬。
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Ceramide induced mitophagy and tumor suppression.神经酰胺诱导线粒体自噬并具有肿瘤抑制作用。
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Targeting cancer stem cells with antibiotics inducing mitochondrial dysfunction as an alternative anticancer therapy.以诱导线粒体功能障碍的抗生素靶向癌症干细胞作为一种替代抗癌疗法。
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Mitophagy is triggered by mild oxidative stress in a mitochondrial fission dependent manner.线粒体自噬由轻度氧化应激以线粒体分裂依赖的方式触发。
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Stress-related mitochondrial components and mitochondrial genome as targets of anticancer therapy.应激相关的线粒体成分和线粒体基因组作为抗癌治疗的靶点。
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