ArticleInternational journal of biological sciences2024
Breast cancer-derived CAV1 promotes lung metastasis by regulating integrin α6β4 and the recruitment and polarization of tumor-associated neutrophils.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Orchestrating the metastatic symphony: the role of extracellular vesicles in the epithelial-mesenchymal transition and pulmonary niche formation of breast cancer.Biological reviews of the Cambridge Philosophical Society · 2026Review
- Extracellular vesicles in breast cancer metastasis: functional insights and advances in single-EV analysis.Cancer metastasis reviews · 2026Review
- Small extracellular vesicles as system-level regulators and predictive biomarkers in breast cancer progression and chemoresistance.Frontiers in pharmacology · 2026Review
- Modulating N1 and N2 neutrophils in breast cancer: potential therapeutic approaches - a narrative review.Annals of medicine and surgery (2012) · 2026Review
- The CCL2-CCR2 axis in primary lung cancer and pulmonary metastasis: from molecular mechanisms to therapeutic potentials.Frontiers in immunology · 2026Review
- N1 and N2 neutrophil subtypes in breast cancer: functional implications and clinical perspectives: a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Biomimetic tumor cell membrane-camouflaged nanomicelles for synergistic chemo-immunotherapy of Triple-negative breast cancer.Materials today. Bio · 2025Article
- Single-cell RNA sequencing technology was employed to construct a risk prediction model for genes associated with pyroptosis and ferroptosis in lung adenocarcinoma.Respiratory research · 2025Article
- Unveiling the Involvement of Extracellular Vesicles in Breast Cancer's Organotrophic Metastasis: Molecular Mechanisms and Translational Prospects.International journal of molecular sciences · 2025Review
- Review
- Role of Triple-Negative Breast Cancer-Derived Extracellular Vesicles in Metastasis: Implications for Therapeutics and Biomarker Development.Journal of cellular and molecular medicine · 2025Review
- Role of toll-like receptors in pulmonary immunity: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- N2 Neutrophils and Tumor Progression in Breast Cancer: Molecular Pathways and Implications.Breast cancer (Dove Medical Press) · 2025Review
- Integrating zinc homeostasis network and immune landscape: a five-gene prognostic framework for precision oncology in lung adenocarcinoma.Frontiers in immunology · 2025Article
- Metabolic reprogramming of tumor-associated neutrophils in tumor treatment and therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung metastasis in breast cancer (BC) patients is one of the main reasons for their high mortality rate. The most prevalent BC small extracellular vesicles (sEVs receptor, integrin α6β4, has been found to interact with surfactant-associated protein (SFTPC) in lung epithelial cells, making BC more likely to metastasize to the lung. Tumor-associated neutrophils (TANs) play an essential role in BC lung metastasis as a component of the lung pre-metastatic niche (PMN) with two sides. It has been demonstrated that Toll-like Receptor4 (TLR4) can participate in signaling, such as NF-B and NLRP3, to facilitate tumor metastasis. A cellular membrane structural protein called caveolin-1 (CAV1) is associated with BC's proliferation, metastasis, and immunological control. According to our previous research, CAV1 on BC-derived sEVs facilitates the formation of the lung PMN by enhancing tenascin-C (TnC) secretion in lung fibroblasts to promote the deposition of ECM, by increasing the expression of PMN marker genes and inflammatory chemokines in lung epithelial cells, and by supporting N2-type polarization of lung macrophages via inhibiting the PTEN/CCL2/VEGF-A axis. More research is needed to determine how sEVs-mediated CAV1 facilitates BC-targeted metastasis to the lungs. By creating a stable-translocating cell line that stably interfered with CAV1 and a mouse model of BC lung metastasis, we investigated how sEVs-mediated CAV1 promotes BC lung metastasis and TAN recruitment and polarization
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