ArticleInternational journal of molecular sciences2023
CCL2-Mediated Stromal Interactions Drive Macrophage Polarization to Increase Breast Tumorigenesis.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- From mechanism to therapy: advances in macrophage polarisation and targeted intervention in osteosarcoma.Frontiers in immunology · 2026Pooled it
- A hereditary rat model of umbilical hernia: characterization, susceptibility locus mapping, and mechanism exploration.iScience · 2026Article
- Molecular Dynamics of Trogocytosis and Other Contact-Dependent Cell Trafficking Mechanisms in Tumor Pathogenesis.Cancers · 2025Review
- Enhanced antitumor immunity of VNP20009-CCL2-CXCL9 via the cGAS/STING axis in osteosarcoma lung metastasis.Journal for immunotherapy of cancer · 2025Article
- Tumor-Associated Macrophage in Breast Tumor Microenvironment.International journal of molecular sciences · 2025Review
- PTPN2 Negatively Regulates Macrophage Immune Responses and Cellular Bioenergetics.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- CD105Breast cancer research : BCR · 2025Article
- Circulating CD3Cancer medicine · 2025Article
- Chemokines as key mediators in RIPI: pathophysiology and translational potential.Frontiers in immunology · 2025Review
- The Laws of Attraction: Chemokines as Critical Mediators in Cancer Progression and Immunotherapy Response in Bladder Cancer.Cancers · 2024Review
- Research progress on the role of tumor‑associated macrophages in tumor development and their use as molecular targets (Review).International journal of oncology · 2024Review
- Unveiling the contribution of tumor-associated macrophages in driving epithelial-mesenchymal transition: a review of mechanisms and therapeutic Strategies.Frontiers in pharmacology · 2024Review
- Recent Advances in Breast Cancer Research.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
CCL2 is an inflammatory cytokine that regulates macrophage activity and is implicated in increased mammographic density and early breast tumorigenesis. The role of CCL2 in mediating stromal interactions that contribute to breast tumorigenesis has yet to be fully elucidated. THP-1-derived macrophages and mammary fibroblasts were co-cultured for 72 h. Fibroblasts and macrophages were analysed for phenotype, expression of inflammatory and ECM-regulatory genes and collagen production. Mice overexpressing CCL2 in the mammary glands were analysed for global gene expression by RNAseq at 12 weeks of age. These mice were cross-bred with PyMT mammary tumour mice to examine the role of CCL2 in tumorigenesis. The co-culture of macrophages with fibroblasts resulted in macrophage polarization towards an M2 phenotype, and upregulated expression of CCL2 and other genes associated with inflammation and ECM remodelling. CCL2 increased the production of insoluble collagen by fibroblasts. A global gene expression analysis of CCL2 overexpressing mice revealed that CCL2 upregulates cancer-associated gene pathways and downregulates fatty acid metabolism gene pathways. In the PyMT mammary tumour model, CCL2 overexpressing mice exhibited increased macrophage infiltration and early tumorigenesis. Interactions between macrophages and fibroblasts regulated by CCL2 can promote an environment that may increase breast cancer risk, leading to enhanced early tumorigenesis.
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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.