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二溴代二苯醚暴露通过细胞外囊泡中的 miR-221 促进三阴性乳腺癌细胞的迁移。

Decarbromodiphenyl ether exposure promotes migration of triple-negative breast cancer cells through miR-221 in extracellular vesicles.

机构信息

Department of Pathology, Wannan Medical College, Wuhu 241002, Anhui Province, China.

出版信息

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2024 Aug 25;53(4):481-489. doi: 10.3724/zdxbyxb-2024-0063.

DOI:10.3724/zdxbyxb-2024-0063
PMID:39183060
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11375496/
Abstract

OBJECTIVES: To investigate the effect of decarbromodiphenyl ether (BDE-209) exposure on the migration ability of triple-negative breast cancer (TNBC) cells and to explore the underlying mechanism. METHODS: Human TNBC MDA-MB-231 cells were divided into blank control group and BDE-209 exposure groups (treated with 0.02, 0.20, 2.00, 20.00 and 200.00 ng/mL BDE-209 in high glucose DMEM). Extracellular vehicles (EVs) secreted by MDA-MB-231 cells were isolated by differential ultracentrifugation. Transmission electron microscopy (SEM), nanoparticle tracking analysis (NTA) and Western blotting were performed to characterize the EVs. The effect of the EVs induced by BDE-209 exposure (EVs-BDE-209) on the migration and invasion of MDA-MB-231 cells was detected by wound-healing assay and Transwell test. qRT-PCR was used to measure the miR-221 level in EVs-BDE-209. The expression of MMP9 in MDA-MB-231 cells was determined by Western blotting. RESULTS: Compared with the blank control, BDE-209 exposure increased the tumor cell-derived EVs in dose-dependent manner. The MDA-MB-231 cells co-cultured with EVs released by 200.00 ng/mL BDE-209 exposure showed an 86% increase in cell migration rate, a 1.32-fold higher number of membrane-penetrating cells, a 2.71-fold higher expression level of miR-221, and a 1.62-fold higher expression level of MMP9 compared with the blank control group (all <0.05). While transfection with anti-miR-221 antibody to decrease miR-221 level in EVs significantly reversed the increased invasion ability of the MDA-MB-231 cells treated with EVs-BDE-209. CONCLUSIONS: BDE-209 exposure may promote metastasis potential of MDA-MB-231 cells via EVs-BDE-209 transmitted miR-221.

摘要

目的：研究十溴联苯醚（BDE-209）暴露对三阴性乳腺癌（TNBC）细胞迁移能力的影响，并探讨其潜在机制。

方法：将人 TNBC MDA-MB-231 细胞分为空白对照组和 BDE-209 暴露组（分别用 0.02、0.20、2.00、20.00 和 200.00ng/mL 的 BDE-209 在高糖 DMEM 中处理）。采用差速超速离心法分离 MDA-MB-231 细胞分泌的细胞外囊泡（EVs）。通过透射电子显微镜（SEM）、纳米颗粒跟踪分析（NTA）和 Western blot 对 EVs 进行鉴定。通过划痕愈合试验和 Transwell 试验检测 BDE-209 暴露诱导的 EVs（EVs-BDE-209）对 MDA-MB-231 细胞迁移和侵袭的影响。qRT-PCR 检测 EVs-BDE-209 中的 miR-221 水平。Western blot 检测 MDA-MB-231 细胞中 MMP9 的表达。

结果：与空白对照组相比，BDE-209 暴露呈剂量依赖性增加肿瘤细胞来源的 EVs。与空白对照组相比，与 200.00ng/mL BDE-209 暴露共培养的 MDA-MB-231 细胞的迁移率增加了 86%，穿透细胞数增加了 1.32 倍，miR-221 表达水平增加了 2.71 倍，MMP9 表达水平增加了 1.62 倍（均<0.05）。用抗 miR-221 抗体转染以降低 EVs 中的 miR-221 水平，可显著逆转 EVs-BDE-209 处理的 MDA-MB-231 细胞侵袭能力的增加。

结论：BDE-209 暴露可能通过 EVs-BDE-209 传递的 miR-221 促进 MDA-MB-231 细胞的转移潜能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/0fa8e35e3995/1008-9292-2024-53-4-481-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/426df3bfb9ff/1008-9292-2024-53-4-481-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/0427c321face/1008-9292-2024-53-4-481-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/19a2b06fb3ad/1008-9292-2024-53-4-481-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/df061bd480c1/1008-9292-2024-53-4-481-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/0fa8e35e3995/1008-9292-2024-53-4-481-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/426df3bfb9ff/1008-9292-2024-53-4-481-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/0427c321face/1008-9292-2024-53-4-481-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/19a2b06fb3ad/1008-9292-2024-53-4-481-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/df061bd480c1/1008-9292-2024-53-4-481-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b99a/11375496/0fa8e35e3995/1008-9292-2024-53-4-481-g005.jpg

相似文献

[1]
Decarbromodiphenyl ether exposure promotes migration of triple-negative breast cancer cells through miR-221 in extracellular vesicles.

Zhejiang Da Xue Xue Bao Yi Xue Ban. 2024-8-25

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[3]
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[5]
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[6]
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[7]
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Int J Mol Sci. 2021-1-15

[8]
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Biosci Rep. 2022-1-28

[9]
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Bosn J Basic Med Sci. 2019-2-12

[10]
[JAG1 affects monocytes-macrophages to reshape the pre-metastatic niche of triple-negative breast cancer through LncRNA MALAT1 in exosomes].

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本文引用的文献

[1]
Hypoxic papillary thyroid carcinoma cells-secreted exosomes deliver miR-221-3p to normoxic tumor cells to elicit a pro-tumoral effect by regulating the ZFAND5.

Exp Cell Res. 2023-10-1

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Colorectal cancer cell-derived extracellular vesicles transfer miR-221-3p to promote endothelial cell angiogenesis via targeting suppressor of cytokine signaling 3.

Life Sci. 2021-11-15

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