ArticleCancers2021
Tumor Extracellular Vesicles Regulate Macrophage-Driven Metastasis through CCL5.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 40 citations in OpenAlex.
- Unveiling CCL5: the master regulator of breast cancer progression and immune evasion.Breast cancer research : BCR · 2026Review
- The Multifaceted Role of Extracellular Vesicles in Triple Negative Breast Cancer.International journal of molecular sciences · 2026Review
- Succinate drives breast cancer bone metastasis by activating the HIF1α/YTHDF1/YAP signaling axis to upregulate chemokine CXCL5 and disrupt the bone microenvironment.Apoptosis : an international journal on programmed cell death · 2026Article
- Article
- The chemokine network in triple-negative breast cancer: its role in immune microenvironment regulation, and prospects for targeted therapy.Frontiers in immunology · 2026Review
- Advanced cell-derived drug delivery systems for pulmonary diseases: from bench to bedside.Drug delivery · 2025Review
- [Mechanisms of Exosomes in Lung Cancer Bone Metastasis and Related Clinical Advances].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- IFI30 promotes tumor-associated macrophage infiltration via activation of the ATF3-CCL5 axis in breast cancer.Innovation (Cambridge (Mass.)) · 2025Article
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- Role of the RAB27/SYTL Axis in Tumor Microenvironment Construction.Cancer science · 2025Review
- A silence catalyst: CCL5-mediated intercellular communication in cancer.Archives of toxicology · 2025Review
- Role of Triple-Negative Breast Cancer-Derived Extracellular Vesicles in Metastasis: Implications for Therapeutics and Biomarker Development.Journal of cellular and molecular medicine · 2025Review
- Tumor-derived extracellular vesicles: key drivers of immunomodulation in breast cancer.Frontiers in immunology · 2025Review
- Influencing immunity: role of extracellular vesicles in tumor immune checkpoint dynamics.Experimental & molecular medicine · 2024Review
- IRF5 suppresses metastasis through the regulation of tumor-derived extracellular vesicles and pre-metastatic niche formation.Scientific reports · 2024Article
- Biological Roles and Clinical Applications of Exosomes in Breast Cancer: A Brief Review.International journal of molecular sciences · 2024Review
- Exosomal circRHCG promotes breast cancer metastasis via facilitating M2 polarization through TFEB ubiquitination and degradation.NPJ precision oncology · 2024Article
- An Update of Extracellular Vesicle Involvement in Different Steps of Cancer Metastasis and Targeting Strategies.Current medicinal chemistry · 2024Review
- Extracellular Vesicles in Triple-Negative Breast Cancer: Immune Regulation, Biomarkers, and Immunotherapeutic Potential.Cancers · 2023Review
- Abscopal Effect, Extracellular Vesicles and Their Immunotherapeutic Potential in Cancer Treatment.Molecules (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
purposeTo understand how tumor cells alter macrophage biology once they are recruited to triple-negative breast cancer (TNBC) tumors by CCL5.
methodMouse bone marrow derived macrophage (BMDMs) were isolated and treated with recombinant CCL5 protein alone, with tumor cell conditioned media, or with tumor extracellular vesicles (EVs). Media from these tumor EV-educated macrophages (TEMs) was then used to determine how these macrophages affect TNBC invasion. To understand the mechanism, we assayed the cytokine secretion from these macrophages to determine how they impact tumor cell invasion. Tumor CCL5 expression was varied in tumors to determine its role in regulating macrophage biology through EVs.
resultsTumor EVs are a necessary component for programming naïve macrophages toward a pro-metastatic phenotype. CCL5 expression in the tumor cells regulates both EV biogenesis/secretion/cargo and macrophage EV-education toward a pro-metastatic phenotype. Analysis of the tumor EV-educated macrophages (TEMs) showed secretion of a variety of factors including CXCL1, CTLA-4, IFNG, OPN, HGF, TGFB, and CCL19 capable of remodeling the surrounding tumor stroma and immune infiltrate. Injection of tumor cells with macrophages educated by metastatic tumor cell EVs into mice increased tumor metastasis to the lung.
conclusionThese results demonstrate that tumor-derived EVs are key mediators of macrophage education and likely play a more complex role in modulating tumor therapeutic response by regulating the tumor immune infiltrate.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.