ArticleCancer research2025
Ferroptotic Neutrophils Induce Immunosuppression and Chemoresistance in Breast Cancer.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Ferroptosis in chemotherapy resistance and resensitization in breast cancer: a systematic review of preclinical evidence and translational implications.Frontiers in oncology · 2026Pooled it
- Neutrophil-based immunotherapy: A metabolic lens on mechanisms and therapeutic implications.Clinical and translational medicine · 2026Review
- Ultrasound-based multiregional radiomics nomogram for predicting recurrence in HER2-positive breast cancer.BMC medical imaging · 2026Article
- Ferroptosis in breast cancer: From adipocyte-immune-iron regulation to therapeutic application.Clinical and translational medicine · 2026Review
- Lipid metabolism reprogramming shapes the immune landscape in the tumor microenvironment.Cellular & molecular immunology · 2026Review
- Immune Checkpoint Inhibitors and Immunomodulators for Cancer Immunotherapy: Insights Into Resistance and Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Bcl-xL blockade targets neutrophils and synergizes with chemotherapy in lung squamous cell carcinoma.EMBO molecular medicine · 2026Article
- Therapy as a State-Generator: Dynamic Phenotypic Landscapes and Adaptive Stress Circuits in Chemotherapy Resistance of Breast Cancer.Antioxidants (Basel, Switzerland) · 2026Review
- Single-cell landscape of intratumoral heterogeneity and GABA-mediated remodeling of the immune microenvironment in breast cancer metastases.Breast cancer research : BCR · 2026Article
- NAC and DNase I synergistically reduce NETs to attenuate severe acute pancreatitis via suppressing the NETs/NF-κB/CXCL3 pathway.Apoptosis : an international journal on programmed cell death · 2026Article
- Metal homeostasis as a therapeutic lever: advancing metalloimmunology to remodel the tumor microenvironment and enhance cancer immunotherapy.Theranostics · 2026Review
- Bidirectional regulation between ferroptosis and tumor-associated macrophages: mechanisms, strategies, and therapeutic perspectives.Frontiers in oncology · 2026Review
- Immune cells dying from ferroptosis: mechanisms and therapeutic opportunities.Cell death & disease · 2025Review
- Co-targeting ferroptosis and immune evasion through small molecules in breast cancer.Journal of translational internal medicine · 2025Article
- Integrated scRNA-seq and transcriptome analyses uncover the effects of UBE2H on the immune microenvironment regulation in pancreatic cancer.Cancer cell international · 2025Article
- Neutrophils and neutrophil extracellular traps: double-edged swords in cancer pathophysiology and therapy resistance.Cell communication and signaling : CCS · 2025Review
- Targeting metalloptosis in tumor therapy: from molecular mechanisms to application of metal nanoparticles.Molecular cancer · 2025Review
- Turning cold tumors into hot tumors to ignite immunotherapy.Molecular cancer · 2025Review
- Co-Targeting PD-1 and IL-33/ST2 Pathways for Enhanced Acquired Anti-Tumor Immunity in Breast Cancer.International journal of molecular sciences · 2025Article
- Natural Compounds as Modulators of Ferroptosis: Mechanistic Insights and Therapeutic Prospects in Breast Cancer.Biomolecules · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Inducing ferroptosis in tumor cells is emerging as a strategy for treating malignancies that are refractory to traditional treatment modalities. However, the consequences of ferroptosis of immune cells in the tumor microenvironment need to be better understood in order to realize the potential of this approach. In this study, we discovered that neutrophils in chemoresistant breast cancer are highly sensitive to ferroptosis. Reduction of the acyltransferase MOAT1 in chemoresistance-associated neutrophils induced phospholipid reprogramming, switching the preference from monounsaturated fatty acids to polyunsaturated fatty acids, which increased their susceptibility to ferroptosis. Ferroptotic neutrophils secreted PGE2, IDO, and oxidized lipids that suppressed the proliferation and cytotoxicity of antitumor CD8+ T cells. Furthermore, neutrophil ferroptosis was closely related to a distinct subset of IL1β+CXCL3+CD4+ (Fer-CD4) T lymphocytes, which were enriched in chemoresistant tumors. Fer-CD4 T cells orchestrated neutrophil ferroptosis by modulating MOAT1 expression via IL1β/IL1R1/NF-κB signaling. Moreover, Fer-CD4 T cells secreted CXCL3, IL8, and S100A9 to replenish the neutrophil pool in the tumor microenvironment. Ferroptotic neutrophils in turn fostered Fer-CD4 T-cell differentiation. In spontaneous tumorigenesis mouse models, targeting IL1β+ CD4+ T cells or IL1R1+ neutrophils broke the cross-talk, restraining neutrophil ferroptosis, enhancing antitumor immunity, and overcoming chemoresistance. Overall, these findings uncover the role of neutrophil ferroptosis in shaping the immune landscape and propose appealing targets for restoring immunosurveillance and chemosensitivity in breast cancer. Significance: In chemoresistant breast cancer, IL1β+CXCL3+CD4+ T cells mediate neutrophil ferroptosis that suppresses antitumor immunity, indicating that interfering with this intercellular cross-talk could be an attractive strategy to reverse chemoresistance.
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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.