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硼簇护送阿霉素挤进外泌体并克服耐药性。

Boron Clusters Escort Doxorubicin Squashing Into Exosomes and Overcome Drug Resistance.

作者信息

Bao Yi-Ru, Chen Yi-Jing, Deng Xue-Fan, Wang Yi-Ke, Zhang Yu-Xin, Xu Li-Li, Huang Wei-Hua, Cheng Shi-Bo, Zhang Hai-Bo, Xie Min

机构信息

College of Chemistry and Molecular Sciences, Wuhan University, 299 Bayi Road, Wuhan, 430072, P. R. China.

College of Chemistry and Molecular Sciences, Engineering Research Center of Organosilicon Compounds & Materials, Ministry of Education and National Demonstration Center for Experimental Chemistry, Wuhan University, 299 Bayi Road, Wuhan, 430072, P. R. China.

出版信息

Adv Sci (Weinh). 2025 Feb;12(7):e2412501. doi: 10.1002/advs.202412501. Epub 2024 Dec 25.

DOI:10.1002/advs.202412501
PMID:39721006
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11831453/
Abstract

Exosome-based drug delivery holds significant promise for cancer chemotherapy. However, current methods for loading drugs into exosomes are inefficient and cost-prohibitive for practical application. In this study, boron clusters are mixed with doxorubicin (DOX) and exosomes, enabling the efficient encapsulation of DOX into exosomes through a superchaotropic effect. Exosomes loaded with DOX and boron clusters (EDB) exhibit superior permeability and the ability to deliver higher concentrations of DOX into DOX-resistant breast cancer cells. Mechanistic analysis reveals that boron clusters form a supramolecular complex with DOX, which facilitates sustained drug release and effectively inhibits P-glycoprotein-mediated DOX efflux. As a result, EDB significantly enhance apoptosis in DOX-resistant breast cancer cells and suppress tumor growth in cases where DOX alone is ineffective, thereby extending the survival of nude mice. In summary, boron clusters effectively facilitate the incorporation of DOX into exosomes and inhibit DOX efflux, offering a novel strategy to overcome DOX resistance.

摘要

基于外泌体的药物递送在癌症化疗方面具有巨大潜力。然而，目前将药物载入外泌体的方法效率低下，且在实际应用中成本过高。在本研究中，硼簇与阿霉素（DOX）和外泌体混合，通过超强离液效应实现DOX在外泌体中的高效包封。负载DOX和硼簇的外泌体（EDB）表现出卓越的渗透性，以及将更高浓度的DOX递送至耐DOX乳腺癌细胞的能力。机制分析表明，硼簇与DOX形成超分子复合物，这有助于药物持续释放，并有效抑制P-糖蛋白介导的DOX外排。结果，EDB显著增强耐DOX乳腺癌细胞的凋亡，并在单独使用DOX无效的情况下抑制肿瘤生长，从而延长裸鼠的生存期。总之，硼簇有效地促进DOX载入外泌体并抑制DOX外排，为克服DOX耐药性提供了一种新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/211ac184a487/ADVS-12-2412501-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/70d448ef5f86/ADVS-12-2412501-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/1cf7a0741d53/ADVS-12-2412501-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/093ddb3e2768/ADVS-12-2412501-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/e4dfbdb6084b/ADVS-12-2412501-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/56e9280fb5a0/ADVS-12-2412501-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/dc210f91dbef/ADVS-12-2412501-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/211ac184a487/ADVS-12-2412501-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/70d448ef5f86/ADVS-12-2412501-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/1cf7a0741d53/ADVS-12-2412501-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/093ddb3e2768/ADVS-12-2412501-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/e4dfbdb6084b/ADVS-12-2412501-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/56e9280fb5a0/ADVS-12-2412501-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/dc210f91dbef/ADVS-12-2412501-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f62/11831453/211ac184a487/ADVS-12-2412501-g002.jpg

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