肿瘤微环境在双链断裂 DNA 损伤反应中新兴的调控作用。
An Emerging Regulatory Role for the Tumor Microenvironment in the DNA Damage Response to Double-Strand Breaks.
机构信息
Department of Pathology, The University of Alabama at Birmingham, Birmingham, Alabama.
O'Neal Comprehensive Cancer Center, The University of Alabama at Birmingham, Birmingham, Alabama.
出版信息
Mol Cancer Res. 2020 Feb;18(2):185-193. doi: 10.1158/1541-7786.MCR-19-0665. Epub 2019 Nov 1.
Abstract
Radiation, alkylating agents, and platinum-based chemotherapy treatments eliminate cancer cells through the induction of excessive DNA damage. The resultant DNA damage challenges the cancer cell's DNA repair capacity. Among the different types of DNA damage induced in cells, double-strand breaks (DSB) are the most lethal if left unrepaired. Unrepaired DSBs in tumor cells exacerbate existing gene deletions, chromosome losses and rearrangements, and aberrant features that characteristically enable tumor progression, metastasis, and drug resistance. Tumor microenvironmental factors like hypoxia, inflammation, cellular metabolism, and the immune system profoundly influence DSB repair mechanisms. Here, we put into context the role of the microenvironment in governing DSB repair mechanisms.
摘要
辐射、烷化剂和基于铂的化疗通过诱导过度的 DNA 损伤来消除癌细胞。由此产生的 DNA 损伤挑战了癌细胞的 DNA 修复能力。在细胞中诱导的不同类型的 DNA 损伤中，如果不修复，双链断裂 (DSB) 是最致命的。肿瘤细胞中未修复的 DSB 会加剧现有基因缺失、染色体丢失和重排以及异常特征，这些特征通常使肿瘤能够进展、转移和产生耐药性。肿瘤微环境因素，如缺氧、炎症、细胞代谢和免疫系统，深刻地影响 DSB 修复机制。在这里，我们将微环境在调控 DSB 修复机制中的作用置于上下文中。
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3
Mismatch repair deficiency/microsatellite instability-high as a predictor for anti-PD-1/PD-L1 immunotherapy efficacy.
J Hematol Oncol. 2019 May 31;12(1):54. doi: 10.1186/s13045-019-0738-1.
4
Natural killer group 2D receptor and its ligands in cancer immune escape.
Mol Cancer. 2019 Feb 27;18(1):29. doi: 10.1186/s12943-019-0956-8.
5
ROS and the DNA damage response in cancer.
Redox Biol. 2019 Jul;25:101084. doi: 10.1016/j.redox.2018.101084. Epub 2018 Dec 21.
6
Nuclear cGAS suppresses DNA repair and promotes tumorigenesis.
Nature. 2018 Nov;563(7729):131-136. doi: 10.1038/s41586-018-0629-6. Epub 2018 Oct 24.
7
Overcoming tumor hypoxia as a barrier to radiotherapy, chemotherapy and immunotherapy in cancer treatment.
Int J Nanomedicine. 2018 Oct 4;13:6049-6058. doi: 10.2147/IJN.S140462. eCollection 2018.
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Pyruvate kinase M2 regulates homologous recombination-mediated DNA double-strand break repair.
Cell Res. 2018 Nov;28(11):1090-1102. doi: 10.1038/s41422-018-0086-7. Epub 2018 Oct 8.
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ROS-induced R loops trigger a transcription-coupled but BRCA1/2-independent homologous recombination pathway through CSB.
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