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细胞外囊泡:新分类与肿瘤免疫抑制

Extracellular Vesicles: New Classification and Tumor Immunosuppression.

作者信息

Sheta Mona, Taha Eman A, Lu Yanyin, Eguchi Takanori

机构信息

Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8525, Japan.

Department of Cancer Biology, National Cancer Institute, Cairo University, Cairo 11796, Egypt.

出版信息

Biology (Basel). 2023 Jan 10;12(1):110. doi: 10.3390/biology12010110.

DOI:10.3390/biology12010110
PMID:36671802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9856004/
Abstract

Extracellular vesicles (EVs) are cell-derived membrane-surrounded vesicles carrying various types of molecules. These EV cargoes are often used as pathophysiological biomarkers and delivered to recipient cells whose fates are often altered in local and distant tissues. Classical EVs are exosomes, microvesicles, and apoptotic bodies, while recent studies discovered autophagic EVs, stressed EVs, and matrix vesicles. Here, we classify classical and new EVs and non-EV nanoparticles. We also review EVs-mediated intercellular communication between cancer cells and various types of tumor-associated cells, such as cancer-associated fibroblasts, adipocytes, blood vessels, lymphatic vessels, and immune cells. Of note, cancer EVs play crucial roles in immunosuppression, immune evasion, and immunotherapy resistance. Thus, cancer EVs change hot tumors into cold ones. Moreover, cancer EVs affect nonimmune cells to promote cellular transformation, including epithelial-to-mesenchymal transition (EMT), chemoresistance, tumor matrix production, destruction of biological barriers, angiogenesis, lymphangiogenesis, and metastatic niche formation.

摘要

细胞外囊泡(EVs)是细胞来源的、被膜包围的囊泡,携带各种类型的分子。这些EVs货物常被用作病理生理生物标志物,并传递给受体细胞,其命运通常在局部和远处组织中发生改变。经典的EVs是外泌体、微囊泡和凋亡小体,而最近的研究发现了自噬性EVs、应激性EVs和基质囊泡。在这里,我们对经典和新型EVs以及非EV纳米颗粒进行分类。我们还综述了EVs介导的癌细胞与各种类型肿瘤相关细胞之间的细胞间通讯,如癌症相关成纤维细胞、脂肪细胞、血管、淋巴管和免疫细胞。值得注意的是,癌症EVs在免疫抑制、免疫逃逸和免疫治疗耐药中起关键作用。因此,癌症EVs将热肿瘤转变为冷肿瘤。此外,癌症EVs影响非免疫细胞以促进细胞转化,包括上皮-间质转化(EMT)、化疗耐药、肿瘤基质产生、生物屏障破坏、血管生成、淋巴管生成和转移小生境形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cf9/9856004/6dd8144e3f11/biology-12-00110-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cf9/9856004/dd76c283f0c2/biology-12-00110-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cf9/9856004/6dd8144e3f11/biology-12-00110-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cf9/9856004/dd76c283f0c2/biology-12-00110-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cf9/9856004/6dd8144e3f11/biology-12-00110-g002.jpg

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