Nuclear pore complex protein RANBP2 and related SUMOylation in solid malignancies

IF 6.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Genes & Diseases Pub Date : 2024-09-04 DOI:10.1016/j.gendis.2024.101407
Xinning Yu, Huatao Wu, Zheng Wu, Yangzheng Lan, Wenjia Chen, Bingxuan Wu, Yu Deng, Jing Liu
{"title":"Nuclear pore complex protein RANBP2 and related SUMOylation in solid malignancies","authors":"Xinning Yu, Huatao Wu, Zheng Wu, Yangzheng Lan, Wenjia Chen, Bingxuan Wu, Yu Deng, Jing Liu","doi":"10.1016/j.gendis.2024.101407","DOIUrl":null,"url":null,"abstract":"The growing interest in post-translational protein modification, particularly in SUMOylation, is driven by its crucial role in cell cycle regulation. SUMOylation affects various cell cycle regulators, including oncogenes, suggesting its relevance in cancer. SUMO E3 ligases are pivotal in this process, exhibiting diverse functionalities through structural domains and subcellular localizations. A less-explored SUMO E3 ligase, RANBP2, a component of the vertebrate nuclear pore complex, emerges as a central player in cellular cycle processes, as well as in tumorigenesis. The current studies illuminate the importance of RANBP2 and underscore the need for more extensive studies to validate its clinical applicability in neoplastic interventions. Our review elucidates the significance of RANBP2 across various types of malignancies. Additionally, it delves into exploring RANBP2 as a prospective therapeutic target for cancer treatment, offering insights into the avenues that scholars should pursue in their subsequent research endeavors. Thus, further investigation into RANBP2's role in solid tumorigenesis is eagerly awaited.","PeriodicalId":12689,"journal":{"name":"Genes & Diseases","volume":"40 1","pages":""},"PeriodicalIF":6.9000,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Genes & Diseases","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.gendis.2024.101407","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

The growing interest in post-translational protein modification, particularly in SUMOylation, is driven by its crucial role in cell cycle regulation. SUMOylation affects various cell cycle regulators, including oncogenes, suggesting its relevance in cancer. SUMO E3 ligases are pivotal in this process, exhibiting diverse functionalities through structural domains and subcellular localizations. A less-explored SUMO E3 ligase, RANBP2, a component of the vertebrate nuclear pore complex, emerges as a central player in cellular cycle processes, as well as in tumorigenesis. The current studies illuminate the importance of RANBP2 and underscore the need for more extensive studies to validate its clinical applicability in neoplastic interventions. Our review elucidates the significance of RANBP2 across various types of malignancies. Additionally, it delves into exploring RANBP2 as a prospective therapeutic target for cancer treatment, offering insights into the avenues that scholars should pursue in their subsequent research endeavors. Thus, further investigation into RANBP2's role in solid tumorigenesis is eagerly awaited.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
实体恶性肿瘤中的核孔复合体蛋白 RANBP2 和相关 SUMOylation
蛋白质翻译后修饰,尤其是 SUMOylation,在细胞周期调控中发挥着至关重要的作用,因而越来越受到人们的关注。SUMOylation 会影响包括癌基因在内的各种细胞周期调控因子,这表明它与癌症有关。SUMO E3 连接酶在这一过程中起着关键作用,通过结构域和亚细胞定位表现出多种功能。脊椎动物核孔复合体的一个组成成分 RANBP2 是一种较少被研究的 SUMO E3 连接酶,它在细胞周期过程和肿瘤发生过程中发挥着核心作用。目前的研究阐明了 RANBP2 的重要性,并强调需要进行更广泛的研究来验证其在肿瘤干预中的临床适用性。我们的综述阐明了 RANBP2 在各类恶性肿瘤中的重要性。此外,它还深入探讨了将 RANBP2 作为癌症治疗靶点的前景,为学者们在后续研究工作中应采取的途径提供了启示。因此,我们热切期待着进一步研究 RANBP2 在实体瘤发生中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Genes & Diseases
Genes & Diseases Multiple-
CiteScore
7.30
自引率
0.00%
发文量
347
审稿时长
49 days
期刊介绍: Genes & Diseases is an international journal for molecular and translational medicine. The journal primarily focuses on publishing investigations on the molecular bases and experimental therapeutics of human diseases. Publication formats include full length research article, review article, short communication, correspondence, perspectives, commentary, views on news, and research watch. Aims and Scopes Genes & Diseases publishes rigorously peer-reviewed and high quality original articles and authoritative reviews that focus on the molecular bases of human diseases. Emphasis will be placed on hypothesis-driven, mechanistic studies relevant to pathogenesis and/or experimental therapeutics of human diseases. The journal has worldwide authorship, and a broad scope in basic and translational biomedical research of molecular biology, molecular genetics, and cell biology, including but not limited to cell proliferation and apoptosis, signal transduction, stem cell biology, developmental biology, gene regulation and epigenetics, cancer biology, immunity and infection, neuroscience, disease-specific animal models, gene and cell-based therapies, and regenerative medicine.
期刊最新文献
Targeting MYC: Multidimensional regulation and therapeutic strategies in oncology Heavy mechanical force decelerates orthodontic tooth movement via Piezo1-induced mitochondrial calcium down-regulation MAFB-mediated CEBPA regulated human urothelium growth through Wnt/β-catenin signaling pathway HMGN2 accelerates the proliferation and cell cycle progression of glioblastoma by regulating CDC20 expression Systematic pan-cancer analysis identifies DNASE2 as a potential prognostic marker and immunotherapeutic target for glioblastoma multiforme
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1