Cancer drug resistance: redox resetting renders a way.

Cancer drug resistance: redox resetting renders a way.
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癌症耐药性:氧化还原重置提供了一种方法

DOI:
10.18632/oncotarget.8600
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发表时间:
2016-07-05
期刊:
影响因子:
--
通讯作者:
Lei Y
Lei Y
中科院分区:
其他
文献类型:
--
作者:
Liu Y;Li Q;Zhou L;Xie N;Nice EC;Zhang H;Huang C;Lei Y

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氧化还原稳态的破坏是耐药性发展的关键因素,这是当前癌症治疗面临的主要问题。与正常细胞相比,肿瘤细胞通常表现出更高水平的活性氧(ROS),这可以促进肿瘤的进展和发展。在药物治疗后,一些肿瘤细胞可以经历“氧化还原重置”的过程,以获得新的氧化还原平衡,具有更高水平的ROS积累和更强的抗氧化系统。越来越多的证据表明,“氧化还原重置”通过多种机制使癌细胞对抗癌药物产生耐药性,包括增加药物外排速率、改变药物代谢和药物靶点、激活促生存途径和无效诱导细胞死亡。在这篇文章中,我们提供了深入了解的作用,“氧化还原重置”的耐药性的出现,可能有助于耐药性的药理学调制。
Disruption of redox homeostasis is a crucial factor in the development of drug resistance, which is a major problem facing current cancer treatment. Compared with normal cells, tumor cells generally exhibit higher levels of reactive oxygen species (ROS), which can promote tumor progression and development. Upon drug treatment, some tumor cells can undergo a process of ‘Redox Resetting’ to acquire a new redox balance with higher levels of ROS accumulation and stronger antioxidant systems. Evidence has accumulated showing that the ‘Redox Resetting’ enables cancer cells to become resistant to anticancer drugs by multiple mechanisms, including increased rates of drug efflux, altered drug metabolism and drug targets, activated prosurvival pathways and inefficient induction of cell death. In this article, we provide insight into the role of ‘Redox Resetting’ on the emergence of drug resistance that may contribute to pharmacological modulation of resistance.
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