ArticleNature communications2024
Elevated extracellular matrix protein 1 in circulating extracellular vesicles supports breast cancer progression under obesity conditions.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Spatiotemporal dynamics of the host-tumor metabolic interface: Implications for precision nutritional oncology.Genes & diseases · 2026Review
- Systemic health impact of cancer-associated extracellular vesicles and particles.Nature reviews. Cancer · 2026Review
- Review
- Senescent obesity signature in breast cancer: a paradigm of reverse cardio-oncology.European heart journal · 2026Review
- Cell Surface Deazaflavin-Diazirine Energy-Transfer (DarT) Photoproximity Labeling Using Antibody Conjugates.Bioconjugate chemistry · 2026Article
- Extracellular matrix microarchitecture modulates cellular behavior and extracellular vesicle phenotypes in biomimetic tendon models.Bioengineering & translational medicine · 2026Article
- From cell lines to the clinic: identifying a urinary BlCa-EV signature through comparative proteomics of bladder cancer lysates and extracellular vesicles.Cell communication and signaling : CCS · 2026Article
- Early-activated extracellular matrix proteins shape the metabolic and spatial dynamics of the kidney fibrotic microenvironment.Nature metabolism · 2026Article
- H19 enhances pancreatic cancer proliferation and invasion by reducing miR-29c-5p's inhibitory effects on ATF2/ECM1.Scientific reports · 2026Article
- Obesity-induced metabolic reprogramming of the tumor immune microenvironment: mechanisms, spatial niches, and immunotherapy response.Frontiers in immunology · 2026Review
- Small extracellular vesicles as system-level regulators and predictive biomarkers in breast cancer progression and chemoresistance.Frontiers in pharmacology · 2026Review
- New insights into extracellular vesicles in metastatic cancer: From mechanisms to diagnostics and targeted therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Extracellular matrix protein 1 in cancer: multifaceted roles in tumor progression, prognosis, and therapeutic targeting.Archives of pharmacal research · 2025Review
- Reduced JAG1 Expression Through miR-200 Overexpression or Crispr-Cas Mediated Knockout Impairs TNBC Growth and Metastasis.Molecular carcinogenesis · 2025Article
- Immune Microenvironment Dysregulation: A Contributing Factor to Obesity-Associated Male Infertility.Biomedicines · 2025Review
- Multi-omics analysis identifies diagnostic circulating biomarkers and potential therapeutic targets, revealing IQGAP1 as an oncogene in gastric cancer.NPJ precision oncology · 2025Article
- Urinary extracellular vesicle N-glycomics identifies diagnostic glycosignatures for bladder cancer.Nature communications · 2025Article
- Decoding the Role of Insulin-like Growth Factor 1 and Its Isoforms in Breast Cancer.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cargo content in small extracellular vesicles (sEVs) changes under pathological conditions. Our data shows that in obesity, extracellular matrix protein 1 (ECM1) protein levels are significantly increased in circulating sEVs, which is dependent on integrin-β2. Knockdown of integrin-β2 does not affect cellular ECM1 protein levels but significantly reduces ECM1 protein levels in the sEVs released by these cells. In breast cancer (BC), overexpressing ECM1 increases matrix metalloproteinase 3 (MMP3) and S100A/B protein levels. Interestingly, sEVs purified from high-fat diet-induced obesity mice (D-sEVs) deliver more ECM1 protein to BC cells compared to sEVs from control diet-fed mice. Consequently, BC cells secrete more ECM1 protein, which promotes cancer cell invasion and migration. D-sEVs treatment also significantly enhances ECM1-mediated BC metastasis and growth in mouse models, as evidenced by the elevated tumor levels of MMP3 and S100A/B. Our study reveals a mechanism and suggests sEV-based strategies for treating obesity-associated BC.
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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.