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Inhibitors of DNA double-strand break repair at the crossroads of cancer therapy and genome editing

机译：DNA双链抑制剂在癌症治疗和基因组编辑的十字路口中的DNA双链休息修复

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Conventional cancer treatment modalities such as radiation and chemotherapy, cause cancer cell death by inducing DNA damage, particularly DNA strand breaks. Over the years, newer avenues have emerged for overcoming radio/chemoresistance by harnessing repair proteins as targets for small molecule inhibitors. Analysis of genome-wide expression data in cancer subtypes and understanding synthetic lethal interactions among repair pathways are important stepping-stones. Several inhibitors targeting DNA strand break repair proteins have yielded good effects in preclinical studies, and have the potential to be developed as therapeutics in cancer as monotherapy or in combination with radiation and chemotherapy. Furthermore, these small molecule inhibitors can aid in precise genome editing (using CRISPR) by harnessing the differential levels of repair inside cells. Shifting the repair balance towards homology-directed repair using inhibitors of NHEJ or stimulators of HR has yielded promising effects alongside CRISPR in cells and several disease models. In short, DNA strand break repair inhibitors are the forerunners in cancer therapy and genome editing, working in concert with the established artillery in the field.
机译：常规的癌症治疗方式如辐射和化疗，引起癌细胞死亡，诱导DNA损伤，特别是DNA链断裂。多年来，通过利用修复蛋白作为小分子抑制剂的靶点来克服无线电/化学性的新途径。癌症亚型的基因组表达数据分析，并了解修复途径之间的合成致死相互作用是重要的踩踏石。靶向DNA链修复蛋白的几种抑制剂在临床前研究中产生了良好的效果，并且具有潜在的癌症作为单药治疗或与辐射和化疗组合开发的潜力。此外，这些小分子抑制剂可以通过利用内部细胞内部的差异水平来帮助精确的基因组编辑（使用CRISPR）。使用HR的NHEJ或HR刺激剂的抑制剂转移到同源性定向修复的修复平衡已经在细胞和几种疾病模型中伴随着CRISPR的有希望的效果。简而言之，DNA链断裂修复抑制剂是癌症治疗和基因组编辑的先驱，与现场建立的炮兵一起工作。

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