ArticleJournal of experimental & clinical cancer research : CR2024
Chemotherapy-elicited extracellular vesicle CXCL1 from dying cells promotes triple-negative breast cancer metastasis by activating TAM/PD-L1 signaling.
Article in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 26 citations in OpenAlex.
- Triple-Negative Breast Cancer Cells Utilize IL8 and CXCL1 to Suppress NK Cells' Function and Facilitate Cancer Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spatial organization of the TNBC tumor microenvironment: multicellular niches, T-cell bottlenecks, and therapeutic opportunities.Journal of translational medicine · 2026Review
- The Multifaceted Role of Extracellular Vesicles in Triple Negative Breast Cancer.International journal of molecular sciences · 2026Review
- Extracellular vesicles in solid tumors: from tumor ecology to engineered therapeutics.Molecular cancer · 2026Review
- P2RY6Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Integrated pan-cancer analysis and experimental validation reveal that syndecan-1 drives glioblastoma pathogenesis and associates with immune infiltration.Discover oncology · 2026Article
- CXCL1 in triple‑negative breast cancer: Mechanisms, challenges, and therapeutic opportunities (Review).Oncology reports · 2026Review
- Tumor-Associated Macrophage-Derived CXCL1 Promotes Endometrial Cancer Progression Through the CXCR2/NF-κB Pathway.Cancer science · 2026Article
- Biomimetic hybrid membrane-coated nanoparticles loaded with rhein-iron complex enhance ferroptosis and immunotherapy for triple-negative breast cancer.Materials today. Bio · 2026Article
- Remodeling the tumor immune microenvironment: mechanisms of crosstalk between regulated cell death macrophages.Frontiers in immunology · 2026Review
- A novel cuproptosis-related prognostic gene signature and validation of differential expression in colon cancer.Discover oncology · 2025Article
- Spatial Transcriptomics Reveals Transcriptomic and Immune Microenvironment Reprogramming during Thyroid Carcinoma Dedifferentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Extracellular vesicles: biogenesis mechanism and impacts on tumor immune microenvironment.Journal of biomedical science · 2025Review
- Senkyunolide H reverses depression-induced breast cancer progression by regulating CXCR2.Natural products and bioprospecting · 2025Article
- Role of Triple-Negative Breast Cancer-Derived Extracellular Vesicles in Metastasis: Implications for Therapeutics and Biomarker Development.Journal of cellular and molecular medicine · 2025Review
- Effect of Extracellular Vesicles Derived From Tumor Cells on Immune Evasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Article
- Glutamine metabolism and ammonia death: targeted modulation for enhanced cancer immunotherapy.Frontiers in immunology · 2025Review
- Tumor-derived extracellular vesicles: key drivers of immunomodulation in breast cancer.Frontiers in immunology · 2025Review
- Cancer cell-derived extracellular vesicles: a potential target for overcoming tumor immunotherapy resistance and immune evasion strategies.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, and chemotherapy still serves as the cornerstone treatment functioning by inducing cytotoxic cell death. Notably, emerging evidence suggests that dying cell-released signals may induce cancer progression and metastasis by modulating the surrounding microenvironment. However, the underlying molecular mechanisms and targeting strategies are yet to be explored.
methodsApoptotic TNBC cells induced by paclitaxel or adriamycin treatment were sorted and their released extracellular vesicles (EV-dead) were isolated from the cell supernatants. Chemokine array analysis was conducted to identify the crucial molecules in EV-dead. Zebrafish and mouse xenograft models were used to investigate the effect of EV-dead on TNBC progression in vivo.
resultsIt was demonstrated that EV-dead were phagocytized by macrophages and induced TNBC metastasis by promoting the infiltration of immunosuppressive PD-L1
conclusionsOur results highlight CXCL1
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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 Socratic graph.