G protein-coupled receptors: a gateway to targeting oncogenic EVs?

Lotte Di Niro, Amber C. Linders, Thomas Glynn, D. M. Pegtel, M. Siderius, C. Crudden, Martine J. Smit
{"title":"G protein-coupled receptors: a gateway to targeting oncogenic EVs?","authors":"Lotte Di Niro, Amber C. Linders, Thomas Glynn, D. M. Pegtel, M. Siderius, C. Crudden, Martine J. Smit","doi":"10.20517/evcna.2024.10","DOIUrl":null,"url":null,"abstract":"Dysregulated intercellular communication is a key feature driving cancer progression. Recently, extracellular vesicles (EVs) have added a new channel to this dense communication network. Despite solid evidence that EVs are central mediators of dysregulated signaling in onco-pathological settings, this has yet to be translated into clinically actionable strategies. The heterogeneity of EV cargo molecules, plasticity of biogenesis routes, and large overlap with their role in physiological communication, complicate a potential targeting strategy. However, recent work has linked EV biology to perhaps the \"most druggable\" proteins - G protein-coupled receptors (GPCRs). GPCR targeting accounts for ~60% of drugs in development and more than a third of all currently approved drugs, spanning almost all areas of medicine. Although several GPCRs have been linked to cancer initiation and progression, relatively few agents have made it into oncological regimes, suggesting that their potential is underexploited. Herein, we examine the molecular mechanisms linking GPCRs to EV communication in cancer settings. We propose that GPCRs hold potential in the search for EV-targeting in oncology.","PeriodicalId":73008,"journal":{"name":"Extracellular vesicles and circulating nucleic acids","volume":"9 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Extracellular vesicles and circulating nucleic acids","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.20517/evcna.2024.10","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Dysregulated intercellular communication is a key feature driving cancer progression. Recently, extracellular vesicles (EVs) have added a new channel to this dense communication network. Despite solid evidence that EVs are central mediators of dysregulated signaling in onco-pathological settings, this has yet to be translated into clinically actionable strategies. The heterogeneity of EV cargo molecules, plasticity of biogenesis routes, and large overlap with their role in physiological communication, complicate a potential targeting strategy. However, recent work has linked EV biology to perhaps the "most druggable" proteins - G protein-coupled receptors (GPCRs). GPCR targeting accounts for ~60% of drugs in development and more than a third of all currently approved drugs, spanning almost all areas of medicine. Although several GPCRs have been linked to cancer initiation and progression, relatively few agents have made it into oncological regimes, suggesting that their potential is underexploited. Herein, we examine the molecular mechanisms linking GPCRs to EV communication in cancer settings. We propose that GPCRs hold potential in the search for EV-targeting in oncology.
G 蛋白偶联受体:靶向致癌 EV 的通道?
细胞间通讯失调是导致癌症进展的一个关键特征。最近,细胞外囊泡(EVs)为这一密集的通讯网络增添了新的渠道。尽管有确凿证据表明,细胞外囊泡是肿瘤病理环境中信号失调的核心介质,但这尚未转化为临床可操作的策略。EV载货分子的异质性、生物生成途径的可塑性以及与其在生理通讯中的作用的大量重叠,使潜在的靶向策略变得复杂。不过,最近的研究工作已将 EV 生物学与或许是 "最有药用价值 "的蛋白质--G 蛋白偶联受体(GPCR)联系起来。以 GPCR 为靶点的药物约占在研药物的 60%,占目前已批准药物的三分之一以上,几乎涵盖了所有医学领域。虽然有几种 GPCR 与癌症的发生和发展有关,但能用于肿瘤治疗的药物相对较少,这表明它们的潜力尚未得到充分开发。在此,我们研究了癌症环境中连接 GPCR 与 EV 通信的分子机制。我们认为,GPCR 在寻找肿瘤学中的 EV 靶向药物方面具有潜力。
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 求助全文
来源期刊
CiteScore
4.10
自引率
0.00%
发文量
0
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信