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三阴性乳腺癌中外泌体释放潜在抑制剂的广泛研究。

An extensive study of potential inhibitors of extracellular vesicles release in triple-negative breast cancer.

机构信息

School of Pharmacy and Pharmaceutical Sciences, Trinity College Dublin, Dublin, Ireland.

Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.

出版信息

BMC Cancer. 2023 Jul 13;23(1):654. doi: 10.1186/s12885-023-11160-2.

DOI:10.1186/s12885-023-11160-2
PMID:37442985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10339474/
Abstract

BACKGROUND

Cancer cells release heterogeneous populations of extracellular vesicles (EVs) that transmit aggressive phenotypic traits to recipient cells. We aimed to establish if the heterogenous EVs population or a sub-population is responsible, if we could block undesirable cell-to-cell communication by EVs, and, if some EVs continued to be released, would their undesirable influences on recipient cells continue.

METHODS

Three triple-negative breast cancer (TNBC) cell lines were used. Non-toxic concentrations of calpeptin, Y27632, manumycin A, GW4869 and combinations thereof were tested to block EVs. Ultracentrifugation-based methods collected EVs, which were then characterised by nanoparticle tracking analysis, immunoblotting, and transmission electron microscopy. A quick screening flow cytometry method evaluated EVs in solution. The influences of EVs on recipient cells' migration was investigated.

RESULTS

All EV sub-populations were apparently involved in transmitting undesirable phenotypic characteristics. All compounds/combinations significantly (64-98%) reduced EVs' release. Our quick screening broadly reflected our more comprehensive EVs analysis. The 2-36% of EVs that continued to be released caused less transmission to recipient cells, but not on a comparable scale to the reduction of EVs release achieved.

CONCLUSION

Up to 98% inhibition of EVs' release was achieved. To prevent the transmission of undesirable phenotypic traits by EVs, their total inhibition may be necessary.

摘要

背景

癌细胞释放异质群体的细胞外囊泡（EVs），将侵袭性表型特征传递给受体细胞。我们旨在确定异质 EVs 群体或亚群是否负责，如果我们可以阻断 EVs 引起的不良细胞间通讯，以及，如果一些 EVs 继续释放，它们对受体细胞的不良影响是否会继续。

方法

使用三种三阴性乳腺癌（TNBC）细胞系。测试了无毒浓度的 calpeptin、Y27632、manumycin A、GW4869 及其组合以阻断 EVs。基于超速离心的方法收集 EVs，然后通过纳米颗粒跟踪分析、免疫印迹和透射电子显微镜进行表征。快速筛选流式细胞术方法评估溶液中的 EVs。研究了 EVs 对受体细胞迁移的影响。

结果

所有 EV 亚群显然都参与传递不良表型特征。所有化合物/组合均显著（64-98%）降低了 EVs 的释放。我们的快速筛选广泛反映了我们更全面的 EVs 分析。继续释放的 2-36%的 EVs 导致向受体细胞的传递减少，但与实现的 EVs 释放减少程度不成比例。

结论

实现了高达 98%的 EVs 释放抑制。为了防止 EVs 传递不良表型特征，可能需要完全抑制它们。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/aeec390d085d/12885_2023_11160_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/95bd3fd97a68/12885_2023_11160_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/a58aaff3f151/12885_2023_11160_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/c6d2fce452a0/12885_2023_11160_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/6f9cf8e1aee9/12885_2023_11160_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/221e6a664bcd/12885_2023_11160_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/aeec390d085d/12885_2023_11160_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/95bd3fd97a68/12885_2023_11160_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/a58aaff3f151/12885_2023_11160_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/c6d2fce452a0/12885_2023_11160_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/6f9cf8e1aee9/12885_2023_11160_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/221e6a664bcd/12885_2023_11160_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f66/10339474/aeec390d085d/12885_2023_11160_Fig6_HTML.jpg

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