• 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

泛素化调节癌症中的自噬:简单的修饰,有前途的靶点。

Ubiquitination regulates autophagy in cancer: simple modifications, promising targets.

机构信息

Institute of Urinary System Diseases, The Affiliated People's Hospital, Jiangsu University, 8 Dianli Road, Zhenjiang, 212002, China.

Department of Basic Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, 212013, China.

出版信息

J Transl Med. 2024 Oct 31;22(1):985. doi: 10.1186/s12967-024-05565-1.

DOI:10.1186/s12967-024-05565-1
PMID:39482684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11526641/
Abstract

Autophagy is an important lysosomal degradation process that digests and recycles bio-molecules, protein or lipid aggregates, organelles, and invaded pathogens. Autophagy plays crucial roles in regulation of metabolic and oxidative stress and multiple pathological processes. In cancer, the role of autophagy is dual and paradoxical. Ubiquitination has been identified as a key regulator of autophagy that can influence various steps in the autophagic process, with autophagy-related proteins being targeted for ubiquitination, thus impacting cancer progression and the effectiveness of therapeutic interventions. This review will concentrate on mechanisms underlying autophagy, ubiquitination, and their interactions in cancer, as well as explore the use of drugs that target the ubiquitin-proteasome system (UPS) and ubiquitination process in autophagy as part of cancer therapy.

摘要

自噬是一种重要的溶酶体降解过程,可消化和回收生物分子、蛋白质或脂质聚集体、细胞器和入侵的病原体。自噬在代谢和氧化应激以及多种病理过程的调节中起着至关重要的作用。在癌症中,自噬的作用是双重的和矛盾的。泛素化已被确定为自噬的关键调节剂,它可以影响自噬过程的各个步骤,自噬相关蛋白被泛素化,从而影响癌症的进展和治疗干预的效果。本综述将集中讨论自噬、泛素化及其在癌症中的相互作用的机制,并探讨将靶向泛素-蛋白酶体系统 (UPS) 和自噬中泛素化过程的药物用于癌症治疗的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/32cf6018f8be/12967_2024_5565_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/6d6ec63aa1d2/12967_2024_5565_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/df402a5cbd8b/12967_2024_5565_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/06cc2c129c4e/12967_2024_5565_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/0372a4d49541/12967_2024_5565_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/b8d02286fbd3/12967_2024_5565_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/c58322790a44/12967_2024_5565_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/32cf6018f8be/12967_2024_5565_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/6d6ec63aa1d2/12967_2024_5565_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/df402a5cbd8b/12967_2024_5565_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/06cc2c129c4e/12967_2024_5565_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/0372a4d49541/12967_2024_5565_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/b8d02286fbd3/12967_2024_5565_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/c58322790a44/12967_2024_5565_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b918/11526641/32cf6018f8be/12967_2024_5565_Fig7_HTML.jpg

相似文献

1
Ubiquitination regulates autophagy in cancer: simple modifications, promising targets.泛素化调节癌症中的自噬:简单的修饰,有前途的靶点。
J Transl Med. 2024 Oct 31;22(1):985. doi: 10.1186/s12967-024-05565-1.
2
Ubiquitination and deubiquitination: Implications on cancer therapy.泛素化和去泛素化:对癌症治疗的影响。
Biochim Biophys Acta Gene Regul Mech. 2023 Dec;1866(4):194979. doi: 10.1016/j.bbagrm.2023.194979. Epub 2023 Aug 24.
3
Ubiquitin-proteasome system (UPS) as a target for anticancer treatment.泛素-蛋白酶体系统(UPS)作为抗癌治疗的靶点。
Arch Pharm Res. 2020 Nov;43(11):1144-1161. doi: 10.1007/s12272-020-01281-8. Epub 2020 Nov 9.
4
Inhibition of proteasome reveals basal mitochondrial ubiquitination.抑制蛋白酶体可揭示基底线粒体泛素化。
J Proteomics. 2020 Oct 30;229:103949. doi: 10.1016/j.jprot.2020.103949. Epub 2020 Aug 31.
5
Ubiquitination-Proteasome System (UPS) and Autophagy Two Main Protein Degradation Machineries in Response to Cell Stress.泛素-蛋白酶体系统(UPS)和自噬:应对细胞应激的两种主要蛋白质降解机制。
Cells. 2022 Mar 1;11(5):851. doi: 10.3390/cells11050851.
6
Role of the ubiquitin proteasome system in hematologic malignancies.泛素蛋白酶体系统在血液系统恶性肿瘤中的作用。
Immunol Rev. 2015 Jan;263(1):224-39. doi: 10.1111/imr.12236.
7
A patent review of the ubiquitin ligase system: 2015-2018.专利审查的泛素连接酶系统:2015-2018。
Expert Opin Ther Pat. 2018 Dec;28(12):919-937. doi: 10.1080/13543776.2018.1549229. Epub 2018 Nov 23.
8
The Roles of Ubiquitin-Binding Protein Shuttles in the Degradative Fate of Ubiquitinated Proteins in the Ubiquitin-Proteasome System and Autophagy.泛素结合蛋白穿梭在泛素蛋白酶体系统和自噬中对泛素化蛋白的降解命运中的作用。
Cells. 2019 Jan 10;8(1):40. doi: 10.3390/cells8010040.
9
Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.泛素化和去泛素化在癌症中的作用:从机制到新的治疗方法。
Mol Cancer. 2024 Jul 25;23(1):148. doi: 10.1186/s12943-024-02046-3.
10
Eat or be eaten: The autophagic plight of inactive 26S proteasomes.适者生存:无活性26S蛋白酶体的自噬困境。
Autophagy. 2015;11(10):1927-8. doi: 10.1080/15548627.2015.1078961.

引用本文的文献

1
A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.癌症治疗的新时代:靶向蛋白酶体 - Bcl - 2轴。
J Exp Clin Cancer Res. 2025 Aug 21;44(1):246. doi: 10.1186/s13046-025-03505-5.
2
Targeting the MARCH5-MFN2 axis to enhance mitochondrial fusion and sensitize multiple myeloma cells to venetoclax.靶向MARCH5-MFN2轴以增强线粒体融合并使多发性骨髓瘤细胞对维奈托克敏感。
J Transl Med. 2025 Aug 14;23(1):917. doi: 10.1186/s12967-025-06942-0.
3
Molecular regulation by ubiquitin-specific proteases (USPs) in HCC: cell cycle, oncogenic signaling, and beyond.

本文引用的文献

1
Neddylation activated TRIM25 desensitizes triple-negative breast cancer to paclitaxel via TFEB-mediated autophagy.泛素化激活的 TRIM25 通过 TFEB 介导的自噬使三阴性乳腺癌对紫杉醇脱敏。
J Exp Clin Cancer Res. 2024 Jun 26;43(1):177. doi: 10.1186/s13046-024-03085-w.
2
MARCH5 promotes hepatocellular carcinoma progression by inducing p53 ubiquitination degradation.MARCH5 通过诱导 p53 泛素化降解促进肝癌进展。
J Cancer Res Clin Oncol. 2024 Jun 11;150(6):303. doi: 10.1007/s00432-024-05782-7.
3
FAT10 mediates the sorafenib-resistance of hepatocellular carcinoma cells by stabilizing E3 ligase NEDD4 to enhance PTEN/AKT pathway-induced autophagy.
泛素特异性蛋白酶(USP)在肝癌中的分子调控:细胞周期、致癌信号传导及其他方面。
Naunyn Schmiedebergs Arch Pharmacol. 2025 Jul 23. doi: 10.1007/s00210-025-04395-2.
4
The Role and Mechanism of Protein Post‑Translational Modification in Rheumatoid Arthritis.蛋白质翻译后修饰在类风湿关节炎中的作用及机制
J Inflamm Res. 2025 Jul 11;18:9055-9078. doi: 10.2147/JIR.S528487. eCollection 2025.
5
N4BP3 Activates TLR4-NF-κB Pathway in Inflammatory Bowel Disease by Promoting K48-Linked IκBα Ubiquitination.N4BP3通过促进K48连接的IκBα泛素化激活炎症性肠病中的TLR4-NF-κB信号通路。
J Inflamm Res. 2025 Jun 3;18:7167-7181. doi: 10.2147/JIR.S518155. eCollection 2025.
6
MiRNA expression profiling and clinical implications in prostate cancer across various stages.不同阶段前列腺癌中的微小RNA表达谱分析及其临床意义
Sci Rep. 2025 Mar 5;15(1):7771. doi: 10.1038/s41598-025-92091-9.
FAT10通过稳定E3连接酶NEDD4以增强PTEN/AKT途径诱导的自噬,介导肝癌细胞对索拉非尼的耐药性。
Am J Cancer Res. 2024 Apr 15;14(4):1523-1544. doi: 10.62347/EPIT4481. eCollection 2024.
4
SPHK1 potentiates colorectal cancer progression and metastasis via regulating autophagy mediated by TRAF6-induced ULK1 ubiquitination.鞘氨醇激酶 1 通过调节 TRAF6 诱导的 ULK1 泛素化介导的自噬促进结直肠癌的进展和转移。
Cancer Gene Ther. 2024 Mar;31(3):410-419. doi: 10.1038/s41417-023-00711-1. Epub 2023 Dec 22.
5
TRAF6 triggers Mycobacterium-infected host autophagy through Rab7 ubiquitination.肿瘤坏死因子受体相关因子6(TRAF6)通过Rab7泛素化触发感染结核分枝杆菌的宿主自噬。
Cell Death Discov. 2023 Nov 28;9(1):427. doi: 10.1038/s41420-023-01731-4.
6
ATM-CHK2-TRIM32 axis regulates ATG7 ubiquitination to initiate autophagy under oxidative stress.ATM-CHK2-TRIM32 轴调节 ATG7 泛素化以在氧化应激下引发自噬。
Cell Rep. 2023 Nov 28;42(11):113402. doi: 10.1016/j.celrep.2023.113402. Epub 2023 Nov 9.
7
GPCR signaling contributes to immune characteristics of microenvironment and process of EBV-induced lymphomagenesis.G蛋白偶联受体(GPCR)信号传导有助于微环境的免疫特性以及EB病毒诱导的淋巴瘤发生过程。
Sci Bull (Beijing). 2023 Nov 15;68(21):2607-2619. doi: 10.1016/j.scib.2023.09.029. Epub 2023 Sep 22.
8
Mezigdomide plus Dexamethasone in Relapsed and Refractory Multiple Myeloma.美法仑氟芬酰胺联合地塞米松治疗复发难治性多发性骨髓瘤
N Engl J Med. 2023 Sep 14;389(11):1009-1022. doi: 10.1056/NEJMoa2303194. Epub 2023 Aug 30.
9
MARCH7-mediated ubiquitination decreases the solubility of ATG14 to inhibit autophagy.MARCH7介导的泛素化作用降低了ATG14的溶解度,从而抑制自噬。
Cell Rep. 2023 Sep 26;42(9):113045. doi: 10.1016/j.celrep.2023.113045. Epub 2023 Aug 26.
10
Ubiquitination Is a Novel Post-Translational Modification of VMP1 in Autophagy of Human Tumor Cells.泛素化是自噬过程中人肿瘤细胞 VMP1 的一种新型翻译后修饰。
Int J Mol Sci. 2023 Aug 19;24(16):12981. doi: 10.3390/ijms241612981.