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外泌体在消化系统肿瘤血管生成中的研究进展

Research progress of exosomes in the angiogenesis of digestive system tumour.

作者信息

Liu Yuan, Wu Hao, Sang Yaodong, Chong Wei, Shang Liang, Li Leping

机构信息

Department of Gastroenterological Surgery, Shandong Provincial Hospital, Shandong University, Jinan, 250021, Shandong, China.

Department of Gastrointestinal Surgery, Key Laboratory of Engineering of Shandong Province, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Shandong Provincial Hospital, Jinan, 250021, China.

出版信息

Discov Oncol. 2024 Feb 11;15(1):33. doi: 10.1007/s12672-024-00879-4.

Abstract

Malignant tumours of the digestive system cover a wide range of diseases that affect the health of people to a large extent. Angiogenesis is indispensable in the development, and metastasis of tumours, mainly in two ways: occupation or formation. Vessels can provide nutrients, oxygen, and growth factors for tumours to encourage growth and metastasis, so cancer progression depends on simultaneous angiogenesis. Recently, exosomes have been proven to participate in the angiogenesis of tumours. They influence angiogenesis by binding to tyrosine kinase receptors (VEGFR)-1, VEGFR-2, and VEGFR-3 with different affinities, regulating Yap-VEGF pathway, Akt pathway or other signaling pathway. Additionally, exosomes are potential therapeutic vectors that can deliver many types of cargoes to different cells. In this review, we summarize the roles of exosomes in the angiogenesis of digestive system tumours and highlight the clinical application prospects, directly used as targers or delivery vehicles, in antiangiogenic therapy.

摘要

消化系统恶性肿瘤涵盖了广泛的疾病,在很大程度上影响着人们的健康。血管生成在肿瘤的发生发展和转移过程中不可或缺,主要通过两种方式:占据或形成。血管可为肿瘤提供营养、氧气和生长因子,以促进肿瘤生长和转移,因此癌症进展依赖于同时发生的血管生成。近年来,外泌体已被证明参与肿瘤血管生成。它们通过以不同亲和力与酪氨酸激酶受体(VEGFR)-1、VEGFR-2和VEGFR-3结合,调节Yap-VEGF通路、Akt通路或其他信号通路来影响血管生成。此外,外泌体是潜在的治疗载体,可将多种类型的物质传递到不同细胞。在本综述中,我们总结了外泌体在消化系统肿瘤血管生成中的作用,并强调了其在抗血管生成治疗中作为直接靶点或递送载体的临床应用前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9ef/10859358/1a4e97c0cf8c/12672_2024_879_Fig1_HTML.jpg

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