ArticleCancer research2020
The Immunosuppressive Microenvironment in BRCA1-IRIS-Overexpressing TNBC Tumors Is Induced by Bidirectional Interaction with Tumor-Associated Macrophages.
Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Hypoxic cancer stem cell-immune niches in the tumor microenvironment: a Systematic Review of mechanisms and therapeutic implications.Frontiers in immunology · 2026Pooled it
- CD47-mediated efferocytosis in diseases: A comprehensive review.Molecular biology reports · 2026Review
- The dual immune landscape of homologous recombination-deficient tumors: mechanisms and therapeutic implications.Cancer metastasis reviews · 2026Review
- Axitinib promotes stemness and vasculogenic mimicry in triple-negative breast cancer by disrupting THBS1-CD47 axis-mediated endothelial-tumor cell communication.Apoptosis : an international journal on programmed cell death · 2026Article
- Understanding the dual role of granulocyte-macrophage colony-stimulating factor in the lung cancer tumor microenvironment and its therapeutic implications.Translational lung cancer research · 2026Review
- Review
- Circular RNA CLASP1 modulates the GLI1/SNAIL axis and enhances macrophage polarization in breast cancer.Oncogene · 2025Article
- Empowering hypoxia to convert cold tumors into hot tumors for breast cancer immunotherapy.Cell death discovery · 2025Review
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- Macrophage regulation of tumor cell dormancy and the dormant niche: an overview in solid tumors.Cancer metastasis reviews · 2025Review
- Tumor-associated macrophages-induced lncRNA RP11-627G18.1 promotes breast cancer metastasis.Genes and immunity · 2025Article
- eEF2K is a poor prognostic factor and novel molecular target in pancreatic cancer: regulating tumor growth and progression via the tumor microenvironment.Cell death & disease · 2025Article
- Genetically engineered macrophages reverse the immunosuppressive tumor microenvironment and improve immunotherapeutic efficacy in TNBC.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- CD105Breast cancer research : BCR · 2025Article
- Roles of tumor-associated macrophages in triple-negative breast cancer progression.Frontiers in immunology · 2025Review
- Analysis of single-cell and spatial transcriptomics in TNBC cell-cell interactions.Frontiers in immunology · 2025Review
- Tumor microenvironment and immunotherapy for triple-negative breast cancer.Biomarker research · 2024Review
- Integrated analysis reveals prognostic correlation and immune characteristics of a tumor-associated macrophage-based risk signature in triple-negative breast cancer.Translational cancer research · 2024Article
- Macrophages: Key Players in the Battle against Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Review
- Deciphering the performance of macrophages in tumour microenvironment: a call for precision immunotherapy.Journal of hematology & oncology · 2024Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Tumor-associated macrophages (TAM) promote triple-negative breast cancer (TNBC) progression. Here, we report BRCA1-IRIS-overexpressing (IRISOE) TNBC cells secrete high levels of GM-CSF in a hypoxia-inducible factor-1α (HIF1α)- and a NF-κB-dependent manner to recruit macrophages to IRISOE cells and polarize them to protumor M2 TAMs. GM-CSF triggered TGFβ1 expression by M2 TAMs by activating STAT5, NF-κB, and/or ERK signaling. Despite expressing high levels of TGFβ1 receptors on their surface, IRISOE TNBC cells channeled TGFβ1/TβRI/II signaling toward AKT, not SMAD, which activated stemness/EMT phenotypes. In orthotopic and syngeneic mouse models, silencing or inactivating IRIS in TNBC cells lowered the levels of circulating GM-CSF, suppressed TAM recruitment, and decreased the levels of circulating TGFβ1. Coinjecting macrophages with IRISOE TNBC cells induced earlier metastasis in athymic mice accompanied by high levels of circulating GM-CSF and TGFβ1. IRISOE TNBC cells expressed low levels of calreticulin (the "eat me" signal for macrophages) and high levels of CD47 (the "do not eat me" signal for macrophages) and PD-L1 (a T-cell inactivator) on their surface. Accordingly, IRISOE TNBC tumors had significantly few CD8
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