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外泌体通过……抑制树突状细胞活化介导三阴性乳腺癌的免疫逃逸

Exosomal Mediates Immune Evasion in Triple-Negative Breast Cancer by Suppressing Dendritic Cell Activation via .

作者信息

Paierhati Puerkaiti, Ma Binlin, Abudukeremu Muzhapaer

机构信息

Department of Breast and Thyroid Surgery, the Affiliated Cancer Hospital of Xinjiang Medical University, Xinjiang Key Laboratory of Oncology, Urumqi, 830011, China.

The Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, Urumqi, 830011, China.

出版信息

Iran J Public Health. 2025 Jun;54(6):1252-1262. doi: 10.18502/ijph.v54i6.18903.

DOI:10.18502/ijph.v54i6.18903
PMID:40655508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12241752/
Abstract

BACKGROUND

This study investigates the role of exosomal integrin beta-2 () from triple-negative breast cancer (TNBC) cells in modulating immune responses, with a focus on its interaction with Toll-like receptor 4 () in dendritic cells (DCs). This study aimed to understand how contributes to the immunosuppressive tumor microenvironment in TNBC.

METHODS

expression in TNBC tissues and cell lines was analyzed using qPCR and Western blot at the Affiliated Cancer Hospital of Xinjiang Medical University between 2013 and 2015. Knockdown and overexpression models of were established in MDA-MB-231 cells to explore their effects on expression in DCs. Exosomes were isolated from these cells, and DCs were co-cultured with exosomes to measure expression and cytokine secretion using flow cytometry and ELISA.

RESULTS

was overexpressed in TNBC tissues, correlating with poor prognosis. Exosomal from TNBC cells suppressed expression in DCs, leading to impaired DC maturation and reduced cytokine secretion, thus promoting an immunosuppressive microenvironment.

CONCLUSION

Targeting the - axis could enhance anti-tumor immunity in TNBC. holds potential as a biomarker and therapeutic target, suggesting that inhibition of exosomal or restoration of DC function may improve therapeutic outcomes in TNBC.

摘要

背景

本研究调查三阴性乳腺癌(TNBC)细胞来源的外泌体整合素β-2( )在调节免疫反应中的作用,重点关注其与树突状细胞(DCs)中Toll样受体4( )的相互作用。本研究旨在了解 如何促成TNBC中的免疫抑制肿瘤微环境。

方法

2013年至2015年期间,在新疆医科大学附属肿瘤医院使用qPCR和蛋白质免疫印迹法分析TNBC组织和细胞系中的 表达。在MDA-MB-231细胞中建立 的敲低和过表达模型,以探索它们对DCs中 表达的影响。从这些细胞中分离出外泌体,并将DCs与外泌体共培养,使用流式细胞术和酶联免疫吸附测定法测量 表达和细胞因子分泌。

结果

在TNBC组织中过表达,与预后不良相关。TNBC细胞来源的外泌体 抑制DCs中的 表达,导致DC成熟受损和细胞因子分泌减少,从而促进免疫抑制微环境。

结论

靶向 轴可增强TNBC中的抗肿瘤免疫力。 作为生物标志物和治疗靶点具有潜力,这表明抑制外泌体 或恢复DC功能可能改善TNBC的治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/81f6a9f48d1c/IJPH-54-1252-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/3b8d810152dd/IJPH-54-1252-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/33049d4e4fbb/IJPH-54-1252-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/4893affac2d3/IJPH-54-1252-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/81f6a9f48d1c/IJPH-54-1252-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/3b8d810152dd/IJPH-54-1252-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/33049d4e4fbb/IJPH-54-1252-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/4893affac2d3/IJPH-54-1252-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6fa/12241752/81f6a9f48d1c/IJPH-54-1252-g004.jpg

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