ArticleThe Journal of experimental medicine2015
CCL2-induced chemokine cascade promotes breast cancer metastasis by enhancing retention of metastasis-associated macrophages.
Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 420 papers, 1 of them a synthesis that pooled it.
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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
420 citing papers in PubMed, 1 synthesis or guideline pooled it, 651 citations in OpenAlex.
- Reverse Onco-Cardiology: What Is the Evidence for Breast Cancer? A Systematic Review of the Literature.International journal of molecular sciences · 2023Pooled it
- A randomized trial evaluating the association between related gene polymorphism and nausea and vomiting induced by cisplatin multi-day chemotherapy.BMC medical genomics · 2023Trial
- The immune phenotype of circulating tumor cells: from escape mechanisms to immunotherapy navigation.Biomarker research · 2026Review
- KDM4A drives TGCT metastasis by inducing focal adhesion disassembly via STAT1-mediated CCL3 transcriptional activation.Oncogene · 2026Article
- Molecular cartography of breast cancer: decoding genomes, heterogeneity and the tumor microenvironment for personalized targeted therapeutics.Molecular biology reports · 2026Review
- In vitro multi-organ invasion model for exploring cardiac resistance to cancer metastasis.Nature communications · 2026Article
- In vitro effects of tensile strain on cancer-associated and matched normal fibroblasts derived from oral squamous cell carcinoma: an exploratory study.BMC cancer · 2026Article
- Unveiling the Paradoxical Tumor-Suppressive Role of CCL2/CCR2 in Bladder Cancer: A Novel Immunotherapeutic Strategy.Cancers · 2026Article
- Tumor-Associated Macrophages Promote Brain Metastasis.bioRxiv : the preprint server for biology · 2026Article
- Hydrogen suppressed tumor growth during chronic intermittent hypoxia via modulating macrophage polarization.Scientific reports · 2026Article
- Macrophage Plasticity: Phenotypic and Functional Profiles Across Pathological Microenvironments.International journal of molecular sciences · 2026Review
- Dynamic remodeling of amino acid metabolism in tumor-associated macrophages: Fueling immunosuppression, reshaping tumor niches, and unlocking metabolic checkpoints.Journal of advanced research · 2026Review
- Charting spatial ligand-target activity using Renoir.Nature communications · 2026Article
- Tumor-Associated Macrophages (TAMs) in Cancer: Functional Programs, Metastatic Mechanisms, and Therapeutic Targeting.Cancers · 2026Review
- Chemokine-defined macrophage niches establish spatial organization of tumor immunity.Nature immunology · 2026Article
- Population-Based Modeling to Predict Human PK/PD of TAK-500, an Anti-CCR2 Antibody-Drug Conjugate for First-in-Human Study in Cancer Patients.Clinical and translational science · 2026Article
- Article
- The role of tumor-associated macrophages in cancer development and their significance as prognostic markers.Clinical and experimental medicine · 2026Review
- Tumor-associated macrophages in head and neck carcinoma: clinicopathological correlations and implications for immunotherapy.Cancer immunology, immunotherapy : CII · 2026Article
- An EGR1-dependent cascade modulates genome architecture at the CSF1R locus.Nucleic acids research · 2026Article
360 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Pulmonary metastasis of breast cancer cells is promoted by a distinct population of macrophages, metastasis-associated macrophages (MAMs), which originate from inflammatory monocytes (IMs) recruited by the CC-chemokine ligand 2 (CCL2). We demonstrate here that, through activation of the CCL2 receptor CCR2, the recruited MAMs secrete another chemokine ligand CCL3. Genetic deletion of CCL3 or its receptor CCR1 in macrophages reduces the number of lung metastasis foci, as well as the number of MAMs accumulated in tumor-challenged lung in mice. Adoptive transfer of WT IMs increases the reduced number of lung metastasis foci in Ccl3 deficient mice. Mechanistically, Ccr1 deficiency prevents MAM retention in the lung by reducing MAM-cancer cell interactions. These findings collectively indicate that the CCL2-triggered chemokine cascade in macrophages promotes metastatic seeding of breast cancer cells thereby amplifying the pathology already extant in the system. These data suggest that inhibition of CCR1, the distal part of this signaling relay, may have a therapeutic impact in metastatic disease with lower toxicity than blocking upstream targets.
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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.