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消除了货物的骨肉瘤衍生的小细胞外囊泡介导竞争细胞摄取抑制骨肉瘤肺转移。

Cargo-eliminated osteosarcoma-derived small extracellular vesicles mediating competitive cellular uptake for inhibiting pulmonary metastasis of osteosarcoma.

机构信息

Institute of Microsurgery on Extremities, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Department of Orthopaedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

J Nanobiotechnology. 2024 Jun 22;22(1):360. doi: 10.1186/s12951-024-02636-9.

DOI:10.1186/s12951-024-02636-9
PMID:38907233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11193292/
Abstract

Osteosarcoma (OS) derived small extracellular vesicles (OS-sEVs) have been shown to induce the formation of cancer-associated fibroblasts (CAFs), characterized by elevated pro-inflammatory factor expression and enhanced migratory and contractile abilities. These CAFs play a crucial role in priming lung metastasis by orchestrating the pre-metastatic niche (PMN) in the lung. Disrupting the communication between OS-sEVs and lung fibroblasts (LFs) emerges as a potent strategy to hinder OS pulmonary metastasis. Our previously established saponin-mediated cargo-elimination strategy effectively reduces the cancer-promoting ability of tumor-derived small extracellular vesicles (TsEVs) while preserving their inherent targeting capability. In this study, we observed that cargo-eliminated OS-sEVs (CE-sEVs) display minimal pro-tumoral and LFs activation potential, yet retain their ability to target LFs. The uptake of OS-sEVs by LFs can be concentration-dependently suppressed by CE-sEVs, preventing the conversion of LFs into CAFs and thus inhibiting PMN formation and pulmonary metastasis of OS. In summary, this study proposes a potential strategy to prevent LFs activation, PMN formation in the lung, and OS pulmonary metastasis through competitive inhibition of OS-sEVs' function by CE-sEVs.

摘要

骨肉瘤（OS）衍生的小细胞外囊泡（OS-sEVs）已被证明能诱导癌症相关成纤维细胞（CAFs）的形成，其特征是促炎因子表达升高和迁移及收缩能力增强。这些 CAFs 通过在肺部协调预转移微环境（PMN）在启动肺转移中起关键作用。破坏 OS-sEVs 和肺成纤维细胞（LFs）之间的通讯是阻止 OS 肺转移的有效策略。我们之前建立的皂素介导的货物消除策略可有效降低肿瘤衍生小细胞外囊泡（TsEVs）的促癌能力，同时保持其固有的靶向能力。在这项研究中，我们观察到，货物消除的 OS-sEVs（CE-sEVs）显示出最小的促肿瘤和 LF 激活潜能，但保留了其靶向 LF 的能力。LFs 对 OS-sEVs 的摄取可以被 CE-sEVs 浓度依赖性地抑制，从而防止 LFs 转化为 CAFs，从而抑制 PMN 的形成和 OS 的肺转移。总之，本研究提出了一种通过 CE-sEVs 竞争性抑制 OS-sEVs 功能来预防 LFs 激活、PMN 在肺部形成和 OS 肺转移的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/57c100181ecf/12951_2024_2636_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/de305ef5125b/12951_2024_2636_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/08bae3e9dbd2/12951_2024_2636_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/93ebba80a9c8/12951_2024_2636_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/491f60dbbd75/12951_2024_2636_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/75f9b4a38e33/12951_2024_2636_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/57c100181ecf/12951_2024_2636_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/de305ef5125b/12951_2024_2636_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/ecf2c6c999a6/12951_2024_2636_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/f57a6a8e0613/12951_2024_2636_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/08bae3e9dbd2/12951_2024_2636_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/93ebba80a9c8/12951_2024_2636_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/491f60dbbd75/12951_2024_2636_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/75f9b4a38e33/12951_2024_2636_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac80/11193292/57c100181ecf/12951_2024_2636_Fig8_HTML.jpg

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