ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Osteoblast-Derived ECM1 Promotes Anti-Androgen Resistance in Bone Metastatic Prostate Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- An Implantable Scaffold Sequentially Releasing STING Agonist and B7-H3 Antibody for Bone Metastasis Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ENO1 as a Central Regulator Linking Metabolic Reprogramming to Tumor Plasticity.International journal of molecular sciences · 2026Review
- Enolase 1: A paradigm of metabolic enzyme moonlighting in tumorigenesis (Review).International journal of oncology · 2026Review
- H19 enhances pancreatic cancer proliferation and invasion by reducing miR-29c-5p's inhibitory effects on ATF2/ECM1.Scientific reports · 2026Article
- Identification and validation of NETs-related biomarkers in hepatocellular carcinoma through bioinformatics analysis and machine learning algorithms.Discover oncology · 2026Article
- Extracellular matrix protein 1 in cancer: multifaceted roles in tumor progression, prognosis, and therapeutic targeting.Archives of pharmacal research · 2025Review
- 3D Nanofibrillar Matrix Stiffness Modulates Extracellular Vesicle Cargo and Pro-Tumour Functions.Journal of extracellular vesicles · 2025Article
- Osteoblast-Derived ECM1 Promotes Anti-Androgen Resistance in Bone Metastatic Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Acquired resistance to hormonal therapy, particularly enzalutamide (ENZ), remains a significant obstacle in the treatment of advanced bone metastatic prostate cancer. Here, it is demonstrated that under ENZ treatment, osteoblasts in the bone microenvironment secrete increased levels of extracellular matrix protein 1 (ECM1), which affects surrounding prostate cancer cells, promoting tumor cell proliferation and anti-androgen resistance. Mechanistically, ECM1 interacts with the enolase 1 (ENO1) receptor on the prostate cancer cell membrane, leading to its phosphorylation at the Y189 site. This event further recruits adapter proteins including growth factor receptor-bound protein 2 (GRB2) and son of sevenless homolog 1 (SOS1), which activates the downstream mitogen-activated protein kinase (MAPK) signaling pathway to induce anti-androgen resistance. Furthermore, inhibiting ECM1 or utilizing the ENO1-targeting inhibitor phosphonoacetohydroxamate (PhAH) significantly restores tumor cell sensitivity to ENZ. Taken together, a potential mechanism is identified through which osteoblast-derived ECM1 drives resistance in bone metastatic prostate cancer under ENZ treatment. Additionally, the findings indicate that ECM1 and ENO1 may serve as potential targets for developing therapies for bone metastatic castration-resistant prostate cancer.
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Registered trials
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