隧道纳米管在肝内胆管癌中花生四烯酸转移和巨噬细胞功能重编程中的作用。

IF 14.1 1区 材料科学 Q1 CHEMISTRY, MULTIDISCIPLINARY
Meiru Chen, Shangyumeng Zhao, Xiaoli Xie, Jiaqi Wang, Miao Su, Lixian Zhang, Ruolin Cui, Dongqiang Zhao
{"title":"隧道纳米管在肝内胆管癌中花生四烯酸转移和巨噬细胞功能重编程中的作用。","authors":"Meiru Chen,&nbsp;Shangyumeng Zhao,&nbsp;Xiaoli Xie,&nbsp;Jiaqi Wang,&nbsp;Miao Su,&nbsp;Lixian Zhang,&nbsp;Ruolin Cui,&nbsp;Dongqiang Zhao","doi":"10.1002/advs.202500148","DOIUrl":null,"url":null,"abstract":"<p>Tumor-associated macrophages (TAMs) play a crucial role in tumor progression within the tumor microenvironment (TME) through phenotypic plasticity and functional modulation. While tunneling nanotubes (TNTs) mediate intercellular communication, their role in shaping TAMs phenotypes and function remains unclear. This study explores how TNTs facilitate the transfer of tumor-derived materials, particularly fatty acids, to TAMs, affecting macrophage polarization and function. Single-cell RNA sequencing identified heterogeneous macrophage subpopulations in the TME. Enrichment analysis pinpointed key substances transferred via TNTs. Lipidomics and metabolomics analyzed the fatty acids involved. In vitro and in vivo experiments validated TNTs-mediated material transfer, and transcriptomic analysis revealed the associated signaling pathways. TNTs are the primary route for transferring tumor-derived fatty acids, notably arachidonic acid (AA), to macrophages. This transfer reprogrammed TAMs from anti-tumor CD5L<sup>+</sup> to pro-tumor TREM2<sup>+</sup> phenotypes, increasing CCL18 secretion, reducing phagocytic activity, and impairing CD8<sup>+</sup> T cell proliferation. Mechanistically, AA activated the PI3K-AKT pathway, driving TAMs polarization. These findings are confirmed in xenograft models, where TNTs-induced TAMs exhibited enhanced pro-tumor properties. TNTs-mediated transfer of tumor-derived AA reprograms TAMs via PI3K-AKT activation, promoting immune suppression and tumor progression, highlighting TNTs and PI3K-AKT as potential therapeutic targets in iCCA.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":"12 35","pages":""},"PeriodicalIF":14.1000,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://advanced.onlinelibrary.wiley.com/doi/epdf/10.1002/advs.202500148","citationCount":"0","resultStr":"{\"title\":\"Role of Tunneling Nanotubes in Arachidonic Acid Transfer and Macrophage Function Reprogramming in Intrahepatic Cholangiocarcinoma\",\"authors\":\"Meiru Chen,&nbsp;Shangyumeng Zhao,&nbsp;Xiaoli Xie,&nbsp;Jiaqi Wang,&nbsp;Miao Su,&nbsp;Lixian Zhang,&nbsp;Ruolin Cui,&nbsp;Dongqiang Zhao\",\"doi\":\"10.1002/advs.202500148\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Tumor-associated macrophages (TAMs) play a crucial role in tumor progression within the tumor microenvironment (TME) through phenotypic plasticity and functional modulation. While tunneling nanotubes (TNTs) mediate intercellular communication, their role in shaping TAMs phenotypes and function remains unclear. This study explores how TNTs facilitate the transfer of tumor-derived materials, particularly fatty acids, to TAMs, affecting macrophage polarization and function. Single-cell RNA sequencing identified heterogeneous macrophage subpopulations in the TME. Enrichment analysis pinpointed key substances transferred via TNTs. Lipidomics and metabolomics analyzed the fatty acids involved. In vitro and in vivo experiments validated TNTs-mediated material transfer, and transcriptomic analysis revealed the associated signaling pathways. TNTs are the primary route for transferring tumor-derived fatty acids, notably arachidonic acid (AA), to macrophages. This transfer reprogrammed TAMs from anti-tumor CD5L<sup>+</sup> to pro-tumor TREM2<sup>+</sup> phenotypes, increasing CCL18 secretion, reducing phagocytic activity, and impairing CD8<sup>+</sup> T cell proliferation. Mechanistically, AA activated the PI3K-AKT pathway, driving TAMs polarization. These findings are confirmed in xenograft models, where TNTs-induced TAMs exhibited enhanced pro-tumor properties. TNTs-mediated transfer of tumor-derived AA reprograms TAMs via PI3K-AKT activation, promoting immune suppression and tumor progression, highlighting TNTs and PI3K-AKT as potential therapeutic targets in iCCA.</p>\",\"PeriodicalId\":117,\"journal\":{\"name\":\"Advanced Science\",\"volume\":\"12 35\",\"pages\":\"\"},\"PeriodicalIF\":14.1000,\"publicationDate\":\"2025-06-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://advanced.onlinelibrary.wiley.com/doi/epdf/10.1002/advs.202500148\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advanced Science\",\"FirstCategoryId\":\"88\",\"ListUrlMain\":\"https://advanced.onlinelibrary.wiley.com/doi/10.1002/advs.202500148\",\"RegionNum\":1,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advanced Science","FirstCategoryId":"88","ListUrlMain":"https://advanced.onlinelibrary.wiley.com/doi/10.1002/advs.202500148","RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0

摘要

肿瘤相关巨噬细胞(tumor associated macrophages, tam)通过表型可塑性和功能调节在肿瘤微环境(tumor microenvironment, TME)内的肿瘤进展中起着至关重要的作用。虽然隧道纳米管(TNTs)介导细胞间通讯,但它们在塑造TNTs表型和功能中的作用尚不清楚。本研究探讨了TNTs如何促进肿瘤来源物质(尤其是脂肪酸)向tam的转移,从而影响巨噬细胞的极化和功能。单细胞RNA测序鉴定了TME中异质巨噬细胞亚群。富集分析确定了通过tnt转移的关键物质。脂质组学和代谢组学分析了所涉及的脂肪酸。体外和体内实验验证了tnt介导的物质转移,转录组学分析揭示了相关的信号通路。tnt是将肿瘤来源的脂肪酸,特别是花生四烯酸(AA)转移到巨噬细胞的主要途径。这种转移将tam从抗肿瘤CD5L+表型重编程为促肿瘤TREM2+表型,增加CCL18分泌,降低吞噬活性,并损害CD8+ T细胞增殖。机制上,AA激活PI3K-AKT通路,驱动tam极化。这些发现在异种移植物模型中得到证实,其中tnt诱导的tam表现出增强的促肿瘤特性。TNTs介导的肿瘤源性AA转移通过PI3K-AKT激活对tam进行重编程,促进免疫抑制和肿瘤进展,突出了TNTs和PI3K-AKT作为iCCA的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Role of Tunneling Nanotubes in Arachidonic Acid Transfer and Macrophage Function Reprogramming in Intrahepatic Cholangiocarcinoma

Role of Tunneling Nanotubes in Arachidonic Acid Transfer and Macrophage Function Reprogramming in Intrahepatic Cholangiocarcinoma

Role of Tunneling Nanotubes in Arachidonic Acid Transfer and Macrophage Function Reprogramming in Intrahepatic Cholangiocarcinoma

Role of Tunneling Nanotubes in Arachidonic Acid Transfer and Macrophage Function Reprogramming in Intrahepatic Cholangiocarcinoma

Role of Tunneling Nanotubes in Arachidonic Acid Transfer and Macrophage Function Reprogramming in Intrahepatic Cholangiocarcinoma

Tumor-associated macrophages (TAMs) play a crucial role in tumor progression within the tumor microenvironment (TME) through phenotypic plasticity and functional modulation. While tunneling nanotubes (TNTs) mediate intercellular communication, their role in shaping TAMs phenotypes and function remains unclear. This study explores how TNTs facilitate the transfer of tumor-derived materials, particularly fatty acids, to TAMs, affecting macrophage polarization and function. Single-cell RNA sequencing identified heterogeneous macrophage subpopulations in the TME. Enrichment analysis pinpointed key substances transferred via TNTs. Lipidomics and metabolomics analyzed the fatty acids involved. In vitro and in vivo experiments validated TNTs-mediated material transfer, and transcriptomic analysis revealed the associated signaling pathways. TNTs are the primary route for transferring tumor-derived fatty acids, notably arachidonic acid (AA), to macrophages. This transfer reprogrammed TAMs from anti-tumor CD5L+ to pro-tumor TREM2+ phenotypes, increasing CCL18 secretion, reducing phagocytic activity, and impairing CD8+ T cell proliferation. Mechanistically, AA activated the PI3K-AKT pathway, driving TAMs polarization. These findings are confirmed in xenograft models, where TNTs-induced TAMs exhibited enhanced pro-tumor properties. TNTs-mediated transfer of tumor-derived AA reprograms TAMs via PI3K-AKT activation, promoting immune suppression and tumor progression, highlighting TNTs and PI3K-AKT as potential therapeutic targets in iCCA.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Advanced Science
Advanced Science CHEMISTRY, MULTIDISCIPLINARYNANOSCIENCE &-NANOSCIENCE & NANOTECHNOLOGY
CiteScore
18.90
自引率
2.60%
发文量
1602
审稿时长
1.9 months
期刊介绍: Advanced Science is a prestigious open access journal that focuses on interdisciplinary research in materials science, physics, chemistry, medical and life sciences, and engineering. The journal aims to promote cutting-edge research by employing a rigorous and impartial review process. It is committed to presenting research articles with the highest quality production standards, ensuring maximum accessibility of top scientific findings. With its vibrant and innovative publication platform, Advanced Science seeks to revolutionize the dissemination and organization of scientific knowledge.
×
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:604180095
Book学术官方微信