ArticleScientific reports2025
B cells enhance IL-1 beta driven invasiveness in triple negative breast cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Tumor-intrinsic IFNγ signaling and niche adaptation drive early colonization in ovarian cancer metastasis.Nature communications · 2026Article
- CXCL1 in triple‑negative breast cancer: Mechanisms, challenges, and therapeutic opportunities (Review).Oncology reports · 2026Review
- Temporal tissue dynamics from a spatial snapshot.Nature · 2026Article
- The spatial immune landscape predicts outcome and reveals the central role of tumor-associated macrophages in inflammatory breast cancer biology.Breast cancer research : BCR · 2026Article
- The type 1 and type 3 immune responses underlying the tissue inflammation associated with NOX2 deficiency.Frontiers in immunology · 2026Review
- B-cells in breast cancer: current insights and challenges.Frontiers in oncology · 2026Review
- Antiproliferative effect of Filopaludina bengalensis fluid inducing apoptosis-necroptosis synergy with immunogenic remodelling in triple-negative breast cancer.Scientific reports · 2025Article
- Review
- The Role of Tumor Microenvironment in Triple-Negative Breast Cancer and Its Therapeutic Targeting.Cells · 2025Review
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
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8 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is an aggressive subtype often characterized by high lymphocyte infiltration, including tumor-infiltrating B cells (TIBs). These cells are present even in early stages of TNBC and associated with microinvasion. This study shows that co-culturing TNBC cells with B cells increases Interleukin-1β (IL-1β) expression and secretion. We further show that B cell-induced IL-1β activates NFκB signaling, leading to higher expression of target genes and promoting IL-1β-dependent increases in matrix metalloproteinase (MMP) activity, invasion, and migration. Immunohistochemical analysis of IL-1β and TIBs in triple-negative ductal carcinoma in situ (DCIS, n = 90) and invasive TNBC (n = 171) revealed that in DCIS, TIBs correlated with IL-1β expression and microinvasion, with IL-1β also linked to recurrence. In invasive TNBC, IL-1β expression correlated with TIB density and stage, with high IL-1β levels associated with poorer survival outcomes. These findings suggest that early B cell presence in TNBC can induce IL-1β secretion, enhancing invasion and mobility through IL-1β-NFκB signaling. This highlights the potential of IL-1 inhibitors as preventive and therapeutic options for hormone receptor-negative DCIS and TNBC.
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Registered trials
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