• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

跨损伤 DNA 合成与化疗耐药中 DNA 合成的重新起始

Translesion DNA Synthesis and Reinitiation of DNA Synthesis in Chemotherapy Resistance.

机构信息

Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russia.

Institute of Genetics and Cytology, National Academy of Sciences of Belarus, Minsk, 220072, Republic of Belarus.

出版信息

Biochemistry (Mosc). 2020 Aug;85(8):869-882. doi: 10.1134/S0006297920080039.

DOI:10.1134/S0006297920080039
PMID:33045948
Abstract

Many chemotherapy drugs block tumor cell division by damaging DNA. DNA polymerases eta (Pol η), iota (Pol ι), kappa (Pol κ), REV1 of the Y-family and zeta (Pol ζ) of the B-family efficiently incorporate nucleotides opposite a number of DNA lesions during translesion DNA synthesis. Primase-polymerase PrimPol and the Pol α-primase complex reinitiate DNA synthesis downstream of the damaged sites using their DNA primase activity. These enzymes can decrease the efficacy of chemotherapy drugs, contribute to the survival of tumor cells and to the progression of malignant diseases. DNA polymerases are promising targets for increasing the effectiveness of chemotherapy, and mutations and polymorphisms in some DNA polymerases can serve as additional prognostic markers in a number of oncological disorders.

摘要

许多化疗药物通过损伤 DNA 来阻止肿瘤细胞分裂。Y 家族的 DNA 聚合酶 eta(Pol η)、iota(Pol ι)、kappa(Pol κ)、REV1 和 B 家族的 zeta(Pol ζ)在跨损伤 DNA 合成过程中能够有效地将核苷酸掺入到许多 DNA 损伤部位的对面。引物酶-聚合酶 PrimPol 和 Pol α-引物酶复合物利用其 DNA 引物酶活性在损伤部位的下游重新启动 DNA 合成。这些酶可以降低化疗药物的疗效,促进肿瘤细胞的存活,并促进恶性疾病的进展。DNA 聚合酶是提高化疗效果的有前途的靶点,一些 DNA 聚合酶的突变和多态性可以作为许多肿瘤疾病的附加预后标志物。

相似文献

1
Translesion DNA Synthesis and Reinitiation of DNA Synthesis in Chemotherapy Resistance.跨损伤 DNA 合成与化疗耐药中 DNA 合成的重新起始
Biochemistry (Mosc). 2020 Aug;85(8):869-882. doi: 10.1134/S0006297920080039.
2
DNA polymerase eta: A potential pharmacological target for cancer therapy.DNA 聚合酶 eta:癌症治疗的潜在药物靶点。
J Cell Physiol. 2021 Jun;236(6):4106-4120. doi: 10.1002/jcp.30155. Epub 2020 Nov 13.
3
Translesion synthesis across abasic lesions by human B-family and Y-family DNA polymerases α, δ, η, ι, κ, and REV1.人类 B 族和 Y 族 DNA 聚合酶 α、δ、η、ι、κ 和 REV1 在碱基切除修复中的跨损伤合成。
J Mol Biol. 2010 Nov 19;404(1):34-44. doi: 10.1016/j.jmb.2010.09.015. Epub 2010 Oct 1.
4
Methylation and hydroxymethylation of cytosine alter activity and fidelity of translesion DNA polymerases.胞嘧啶的甲基化和羟甲基化改变了跨损伤 DNA 聚合酶的活性和保真度。
DNA Repair (Amst). 2024 Sep;141:103712. doi: 10.1016/j.dnarep.2024.103712. Epub 2024 Jun 19.
5
Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?抑制诱变跨损伤合成:改善化疗的一种可能策略?
PLoS Genet. 2017 Aug 17;13(8):e1006842. doi: 10.1371/journal.pgen.1006842. eCollection 2017 Aug.
6
Translesion DNA Synthesis and Carcinogenesis.跨损伤 DNA 合成与致癌作用。
Biochemistry (Mosc). 2020 Apr;85(4):425-435. doi: 10.1134/S0006297920040033.
7
Filling gaps in translesion DNA synthesis in human cells.填补人类细胞中跨损伤DNA合成的缺口。
Mutat Res Genet Toxicol Environ Mutagen. 2018 Dec;836(Pt B):127-142. doi: 10.1016/j.mrgentox.2018.02.004. Epub 2018 Feb 23.
8
Translesion DNA polymerases Pol zeta, Pol eta, Pol iota, Pol kappa and Rev1 are not essential for repeat-induced point mutation in Neurospora crassa.跨损伤DNA聚合酶ζ、η、ι、κ和Rev1对于粗糙脉孢菌中的重复诱导点突变并非必不可少。
J Biosci. 2006 Dec;31(5):557-64. doi: 10.1007/BF02708407.
9
Structural basis of Rev1-mediated assembly of a quaternary vertebrate translesion polymerase complex consisting of Rev1, heterodimeric polymerase (Pol) ζ, and Pol κ.Rev1 介导的四聚体脊椎动物跨损伤聚合酶复合物的组装的结构基础,该复合物由 Rev1、异二聚体聚合酶(Pol)ζ 和 Pol κ 组成。
J Biol Chem. 2012 Sep 28;287(40):33836-46. doi: 10.1074/jbc.M112.394841. Epub 2012 Aug 2.
10
Polymerase iota (Pol ι) prevents PrimPol-mediated nascent DNA synthesis and chromosome instability.聚合酶 ι(Pol ι)可防止 PrimPol 介导的新生 DNA 合成和染色体不稳定性。
Sci Adv. 2023 Apr 14;9(15):eade7997. doi: 10.1126/sciadv.ade7997.

引用本文的文献

1
Engineered exosomes: a promising design platform for overcoming cancer therapy resistance.工程化外泌体:一种克服癌症治疗耐药性的有前景的设计平台。
Front Cell Dev Biol. 2025 Aug 6;13:1608480. doi: 10.3389/fcell.2025.1608480. eCollection 2025.
2
Epigenetic Drivers of Chemoresistance in Nucleobase and Nucleoside Analog Therapies.核碱基和核苷类似物疗法中化疗耐药性的表观遗传驱动因素
Biology (Basel). 2025 Jul 9;14(7):838. doi: 10.3390/biology14070838.
3
Clinical outcomes of DNA-damaging agents and DNA damage response inhibitors combinations in cancer: a data-driven review.
DNA损伤剂与DNA损伤反应抑制剂联合应用于癌症的临床疗效:一项数据驱动的综述。
Front Oncol. 2025 Jun 10;15:1577468. doi: 10.3389/fonc.2025.1577468. eCollection 2025.
4
Chromatin assembly factor 1 subunit A promotes TLS pathway by recruiting E3 ubiquitin ligase RAD18 in cancer cells.染色质组装因子1亚基A通过在癌细胞中招募E3泛素连接酶RAD18促进跨损伤合成途径。
Cell Death Dis. 2025 Mar 1;16(1):147. doi: 10.1038/s41419-025-07468-5.
5
Pan-Cancer Analysis of KANK2: Clinical and Molecular Insights into Tumor Progression and Therapeutic Implications.KANK2的泛癌分析:对肿瘤进展的临床和分子见解及治疗意义
J Cancer. 2025 Jan 6;16(4):1149-1166. doi: 10.7150/jca.105098. eCollection 2025.
6
The Catalytic Activity of Human REV1 on Undamaged and Damaged DNA.人类 REV1 在未受损和受损 DNA 上的催化活性。
Int J Mol Sci. 2024 Apr 8;25(7):4107. doi: 10.3390/ijms25074107.
7
Enzymatic Processing of DNA-Protein Crosslinks.DNA-蛋白质交联的酶处理。
Genes (Basel). 2024 Jan 10;15(1):85. doi: 10.3390/genes15010085.
8
Mutations in the DNA polymerase binding pathway affect the immune microenvironment of patients with small-cell lung cancer and enhance the efficacy of platinum-based chemotherapy.DNA聚合酶结合途径中的突变会影响小细胞肺癌患者的免疫微环境,并增强铂类化疗的疗效。
Cancer Innov. 2023 Jul 11;2(6):500-512. doi: 10.1002/cai2.84. eCollection 2023 Dec.
9
Implications of Translesion DNA Synthesis Polymerases on Genomic Stability and Human Health.跨损伤 DNA 合成聚合酶对基因组稳定性和人类健康的影响。
Mol Cell Biol. 2023;43(8):401-425. doi: 10.1080/10985549.2023.2224199. Epub 2023 Jul 13.
10
Can Cisplatin Therapy Be Improved? Pathways That Can Be Targeted.顺铂治疗能否得到改善?可以靶向的途径。
Int J Mol Sci. 2022 Jun 29;23(13):7241. doi: 10.3390/ijms23137241.