• 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

从端粒替代延长相关早幼粒细胞白血病核体途径中鉴定关键蛋白

Identification of Key Proteins from the Alternative Lengthening of Telomeres-Associated Promyelocytic Leukemia Nuclear Bodies Pathway.

作者信息

Armendáriz-Castillo Isaac, Hidalgo-Fernández Katherine, Pérez-Villa Andy, García-Cárdenas Jennyfer M, López-Cortés Andrés, Guerrero Santiago

机构信息

Latin American Network for the Implementation and Validation of Clinical Pharmacogenomics Guidelines (RELIVAF-CYTED), 28001 Madrid, Spain.

Facultade de Ciencias, Universidade da Coruña, 15071 A Coruña, Spain.

出版信息

Biology (Basel). 2022 Jan 25;11(2):185. doi: 10.3390/biology11020185.

DOI:10.3390/biology11020185
PMID:35205052
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8868596/
Abstract

Alternative lengthening of telomeres-associated promyelocytic leukemia nuclear bodies (APBs) are a hallmark of telomere maintenance. In the last few years, APBs have been described as the main place where telomeric extension occurs in ALT-positive cancer cell lines. A different set of proteins have been associated with APBs function, however, the molecular mechanisms behind their assembly, colocalization, and clustering of telomeres, among others, remain unclear. To improve the understanding of APBs in the ALT pathway, we integrated multiomics analyses to evaluate genomic, transcriptomic and proteomic alterations, and functional interactions of 71 APBs-related genes/proteins in 32 Pan-Cancer Atlas studies from The Cancer Genome Atlas Consortium (TCGA). As a result, we identified 13 key proteins which showed distinctive mutations, interactions, and functional enrichment patterns across all the cancer types and proposed this set of proteins as candidates for future ex vivo and in vivo analyses that will validate these proteins to improve the understanding of the ALT pathway, fill the current research gap about APBs function and their role in ALT, and be considered as potential therapeutic targets for the diagnosis and treatment of ALT-positive cancers in the future.

摘要

端粒替代延长相关的早幼粒细胞白血病核体(APBs)是端粒维持的一个标志。在过去几年中,APBs被描述为ALT阳性癌细胞系中端粒延长发生的主要场所。一组不同的蛋白质与APBs功能相关,然而,它们的组装、共定位以及端粒聚集等背后的分子机制仍不清楚。为了更好地理解ALT途径中的APBs,我们整合了多组学分析,以评估来自癌症基因组图谱联盟(TCGA)的32项泛癌图谱研究中71个与APBs相关的基因/蛋白质的基因组、转录组和蛋白质组改变以及功能相互作用。结果,我们鉴定出13种关键蛋白质,它们在所有癌症类型中表现出独特的突变、相互作用和功能富集模式,并提出这组蛋白质作为未来体外和体内分析的候选对象,这些分析将验证这些蛋白质,以增进对ALT途径的理解,填补当前关于APBs功能及其在ALT中的作用的研究空白,并被视为未来诊断和治疗ALT阳性癌症的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/13be97648f08/biology-11-00185-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/e2a22ba05f7c/biology-11-00185-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/701c1ac2bb33/biology-11-00185-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/4292e4214ee2/biology-11-00185-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/83dc3ae97b44/biology-11-00185-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/13be97648f08/biology-11-00185-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/e2a22ba05f7c/biology-11-00185-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/701c1ac2bb33/biology-11-00185-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/4292e4214ee2/biology-11-00185-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/83dc3ae97b44/biology-11-00185-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8a6/8868596/13be97648f08/biology-11-00185-g005.jpg

相似文献

1
Identification of Key Proteins from the Alternative Lengthening of Telomeres-Associated Promyelocytic Leukemia Nuclear Bodies Pathway.从端粒替代延长相关早幼粒细胞白血病核体途径中鉴定关键蛋白
Biology (Basel). 2022 Jan 25;11(2):185. doi: 10.3390/biology11020185.
2
PML induces compaction, TRF2 depletion and DNA damage signaling at telomeres and promotes their alternative lengthening.PML在端粒处诱导压缩、TRF2缺失和DNA损伤信号传导,并促进其替代延长。
J Cell Sci. 2015 May 15;128(10):1887-900. doi: 10.1242/jcs.148296. Epub 2015 Apr 23.
3
Assembly of functional ALT-associated promyelocytic leukemia bodies requires Nijmegen Breakage Syndrome 1.功能性端粒酶逆转录酶相关早幼粒细胞白血病小体的组装需要尼曼匹克氏病C型。
Cancer Res. 2003 May 15;63(10):2589-95.
4
DNA damage induces alternative lengthening of telomeres (ALT) associated promyelocytic leukemia bodies that preferentially associate with linear telomeric DNA.DNA损伤诱导与端粒替代延长(ALT)相关的早幼粒细胞白血病小体,这些小体优先与线性端粒DNA结合。
Cancer Res. 2007 Aug 1;67(15):7072-7. doi: 10.1158/0008-5472.CAN-07-1556. Epub 2007 Jul 24.
5
PML3 interacts with TRF1 and is essential for ALT-associated PML bodies assembly in U2OS cells.PML3 与 TRF1 相互作用,是 U2OS 细胞中 ALT 相关 PML 体组装所必需的。
Cancer Lett. 2010 May 28;291(2):177-86. doi: 10.1016/j.canlet.2009.10.009. Epub 2009 Nov 8.
6
De novo assembly of a PML nuclear subcompartment occurs through multiple pathways and induces telomere elongation.通过多种途径进行 PML 核亚区的从头组装,并诱导端粒延长。
J Cell Sci. 2011 Nov 1;124(Pt 21):3603-18. doi: 10.1242/jcs.084681.
7
PML body meets telomere: the beginning of an ALTernate ending?PML 体与端粒相遇:非经典端粒末端连接的开始?
Nucleus. 2012 May-Jun;3(3):263-75. doi: 10.4161/nucl.20326. Epub 2012 May 1.
8
Pilocytic astrocytomas have telomere-associated promyelocytic leukemia bodies without alternatively lengthened telomeres.毛细胞型星形细胞瘤具有与端粒相关的早幼粒细胞白血病小体,但不存在端粒的替代性延长。
Am J Pathol. 2010 Dec;177(6):2694-700. doi: 10.2353/ajpath.2010.100468. Epub 2010 Oct 29.
9
Identification of candidate alternative lengthening of telomeres genes by methionine restriction and RNA interference.通过甲硫氨酸限制和RNA干扰鉴定端粒候选替代延长基因
Oncogene. 2007 Jul 12;26(32):4635-47. doi: 10.1038/sj.onc.1210260. Epub 2007 Feb 5.
10
Localization of hRad9, hHus1, hRad1, and hRad17 and caffeine-sensitive DNA replication at the alternative lengthening of telomeres-associated promyelocytic leukemia body.人源Rad9、人源Hus1、人源Rad1和人源Rad17的定位以及端粒相关早幼粒细胞白血病小体处对咖啡因敏感的DNA复制
J Biol Chem. 2004 Jun 11;279(24):25849-57. doi: 10.1074/jbc.M312652200. Epub 2004 Apr 9.

引用本文的文献

1
Metabolic pathways of Alternative Lengthening of Telomeres in pan-carcinoma.泛癌中染色体末端端粒延长替代途径的代谢通路
PLoS One. 2025 Feb 21;20(2):e0314012. doi: 10.1371/journal.pone.0314012. eCollection 2025.
2
Beginning at the ends: telomere and telomere-based cancer therapeutics.从末端开始:端粒与基于端粒的癌症治疗方法。
Mol Genet Genomics. 2024 Dec 6;300(1):1. doi: 10.1007/s00438-024-02206-6.
3
Oxidative stress is two-sided in the treatment of acute myeloid leukemia.氧化应激在急性髓细胞性白血病的治疗中具有两面性。

本文引用的文献

1
Identification of key proteins in the signaling crossroads between wound healing and cancer hallmark phenotypes.鉴定伤口愈合和癌症标志性表型信号交汇点的关键蛋白。
Sci Rep. 2021 Aug 26;11(1):17245. doi: 10.1038/s41598-021-96750-5.
2
TRIM28 inhibits alternative lengthening of telomere phenotypes by protecting SETDB1 from degradation.TRIM28通过保护SETDB1不被降解来抑制端粒表型的替代延长。
Cell Biosci. 2021 Jul 30;11(1):149. doi: 10.1186/s13578-021-00660-y.
3
Expression and Prognosis Analysis of SUMOylation Regulators in Oral Squamous Cell Carcinoma Based on High-Throughput Sequencing.
Cancer Med. 2024 May;13(9):e6806. doi: 10.1002/cam4.6806.
4
The close interaction between hypoxia-related proteins and metastasis in pancarcinomas.缺氧相关蛋白与泛癌转移的密切相互作用。
Sci Rep. 2022 Jun 30;12(1):11100. doi: 10.1038/s41598-022-15246-y.
基于高通量测序的口腔鳞状细胞癌中SUMO化修饰调节因子的表达及预后分析
Front Genet. 2021 Jun 29;12:671392. doi: 10.3389/fgene.2021.671392. eCollection 2021.
4
The Role of Non-Specific Interactions in Canonical and ALT-Associated PML-Bodies Formation and Dynamics.非特异性相互作用在经典和 ALT 相关 PML 体形成和动力学中的作用。
Int J Mol Sci. 2021 May 29;22(11):5821. doi: 10.3390/ijms22115821.
5
Measuring nonhomologous end-joining, homologous recombination and alternative end-joining simultaneously at an endogenous locus in any transfectable human cell.在任何可转染的人类细胞中,在一个内源性基因座上同时测量非同源末端连接、同源重组和非同源末端连接。
Nucleic Acids Res. 2021 Jul 21;49(13):e74. doi: 10.1093/nar/gkab262.
6
Nuclear envelope tethering inhibits the formation of ALT-associated PML bodies in ALT cells.核膜连接抑制 ALT 细胞中 ALT 相关 PML 体的形成。
Aging (Albany NY). 2021 Apr 4;13(7):10490-10516. doi: 10.18632/aging.202810.
7
A Role for Human DNA Polymerase λ in Alternative Lengthening of Telomeres.人类 DNA 聚合酶 λ 在端粒的替代延长中的作用。
Int J Mol Sci. 2021 Feb 27;22(5):2365. doi: 10.3390/ijms22052365.
8
PCNA, a focus on replication stress and the alternative lengthening of telomeres pathway.PCNA,关注复制应激和端粒的非经典延长途径。
DNA Repair (Amst). 2021 Apr;100:103055. doi: 10.1016/j.dnarep.2021.103055. Epub 2021 Feb 3.
9
Alternative lengthening of telomeres is a self-perpetuating process in ALT-associated PML bodies.端粒的替代性延长是 ALT 相关的 PML 体中自我维持的过程。
Mol Cell. 2021 Mar 4;81(5):1027-1042.e4. doi: 10.1016/j.molcel.2020.12.030. Epub 2021 Jan 15.
10
The absence of (TCAGGG) repeats in some telomeres, combined with variable responses to NR2F2 depletion, suggest that this nuclear receptor plays an indirect role in the alternative lengthening of telomeres.一些端粒中(TCAGGG)重复序列的缺失,加上对 NR2F2 耗竭的可变反应,表明这种核受体在端粒的替代性延长中起间接作用。
Sci Rep. 2020 Nov 26;10(1):20597. doi: 10.1038/s41598-020-77606-w.