研究动态
Articles below are published ahead of final publication in an issue. Please cite articles in the following format: authors, (year), title, journal, DOI.

肿瘤血管生成和抗血管生成疗法中细胞外囊泡的作用。

Extracellular vesicles in tumor angiogenesis and resistance to anti-angiogenic therapy.

发表日期:2023 Apr 03
作者: Zi-Wu Ye, Zi-Li Yu, Gang Chen, Jun Jia
来源: BIOMEDICINE & PHARMACOTHERAPY

摘要:

肿瘤血管生成在癌症的发展中发挥重要作用,因为它可以提供氧气、营养和生长因子,并且能够促进肿瘤向远处器官扩散。尽管抗血管生成疗法(AAT)已获批用于治疗各种晚期癌症,但由于随着时间的推移会产生抵抗力,这种潜在策略的疗效有限。因此,急需了解抵抗力是如何产生的。细胞产生的外泌体(EVs)是纳米级别的磷脂质包膜囊泡,越来越多的证据表明,肿瘤细胞源性EV(T-EVs)直接将其货物转移给内皮细胞(ECs)以促进肿瘤血管生成。重要的是,最近的研究报道T-EVs可能在AAT的抵抗力发展中起重要作用。此外,研究表明,非肿瘤细胞的EVs在血管生成中也起着作用,尽管涉及的机制仍不完全清楚。在本综述中,我们全面描述了来自各种细胞(包括肿瘤细胞和非肿瘤细胞)的EVs在肿瘤血管生成中的作用。此外,从EVs的角度出发,本综述重点介绍了EVs在AAT中的抵抗作用及其涉及的机制。由于他们在AAT失败中的作用,我们在这里提出了通过抑制T-EVs进一步提高AAT疗效的潜在策略。本文受版权保护。保留所有权利。
Tumor angiogenesis plays an important role in the development of cancer since it allows for the delivery of oxygen, nutrients, and growth factors as well as tumor dissemination to distant organs. Although anti-angiogenic therapy (AAT) has been approved for treating various advanced cancers, this potential strategy has limited efficacy due to resistance over time. Therefore, there is a critical need to understand how resistance develops. Extracellular vesicles (EVs) are nano-sized membrane-bound phospholipid vesicles produced by cells. A growing body of evidences suggest that tumor cell-derived EVs (T-EVs) directly transfer their cargoes to endothelial cells (ECs) to promote tumor angiogenesis. Importantly, recent studies have reported that T-EVs may play a major role in the development of resistance to AAT. Moreover, studies have demonstrated the role of EVs from non-tumor cells in angiogenesis, although the mechanisms involved are still not completely understood. In this review, we provide a comprehensive description of the role of EVs derived from various cells, including tumor cells and non-tumor cells, in tumor angiogenesis. Moreover, from the perspective of EVs, this review focuses on the role of EVs in the resistance to AAT and the mechanisms involved. Due to their role in the failure of AAT, we here proposed potential strategies to further improve the efficacy of AAT by inhibiting T-EVs.This article is protected by copyright. All rights reserved.