ArticleThe Journal of clinical investigation2011
Tumor endothelin-1 enhances metastatic colonization of the lung in mouse xenograft models of bladder cancer.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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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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Who cites it
72 citing papers in PubMed, 109 citations in OpenAlex.
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- MULGONET: An interpretable neural network framework to integrate multi-omics data for cancer recurrence prediction and biomarker discovery.Fundamental research · 2026Article
- Macrophages in the premetastatic and metastatic niche: key functions and therapeutic directions.Journal of translational medicine · 2025Review
- Identification of ECE2 signaling in promoting non-small lung cancer progression through ET1/YAP1/MAGEA3 axis.Scientific reports · 2025Article
- An iron-rich subset of macrophages promotes tumor growth through a Bach1-Ednrb axis.The Journal of experimental medicine · 2024Article
- Endothelin and the tumor microenvironment: a finger in every pie.Clinical science (London, England : 1979) · 2024Review
- Endothelin-1 and Its Role in Cancer and Potential Therapeutic Opportunities.Biomedicines · 2024Review
- Comparison of Absolute Expression and Turnover Number of COX-1 and COX-2 in Human and Rodent Cells and Tissues.Journal of inflammation research · 2022Article
- Animal Models in Bladder Cancer.Biomedicines · 2021Review
- Metabolomic credentialing of murine carcinogen-induced urothelial cancer.Scientific reports · 2021Article
- Androgen Receptor Regulates CD44 Expression in Bladder Cancer.Cancer research · 2021Article
- A Perspective on Therapeutic Pan-Resistance in Metastatic Cancer.International journal of molecular sciences · 2020Review
- Ambrisentan, an endothelin receptor type A-selective antagonist, inhibits cancer cell migration, invasion, and metastasis.Scientific reports · 2020Article
- ET-1 promotes the growth and metastasis of esophageal squamous cell carcinoma via activating PI3K/Akt pathway.Translational cancer research · 2020Article
- Tumor dormancy as an alternative step in the development of chemoresistance and metastasis - clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- Endothelin Receptor Antagonists: Status Quo and Future Perspectives for Targeted Therapy.Journal of clinical medicine · 2020Review
- The pan-therapeutic resistance of disseminated tumor cells: Role of phenotypic plasticity and the metastatic microenvironment.Seminars in cancer biology · 2020Review
- Irreversible and sustained upregulation of endothelin axis during oncogene-associated pancreatic inflammation and cancer.Neoplasia (New York, N.Y.) · 2020Article
- Endothelin-converting enzyme-1c promotes stem cell traits and aggressiveness in colorectal cancer cells.Molecular oncology · 2020Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Many patients with advanced bladder cancer develop lethal metastases to the lung. The vasoconstricting protein endothelin-1 (ET-1) has been implicated in this process, although the mechanism(s) by which it promotes metastasis remains unclear. Here, we have evaluated whether tumor ET-1 expression can serve as a biomarker for lung metastasis and whether it is required for metastatic disease. Evaluation of ET-1 mRNA and protein expression in four patient cohorts revealed that levels of ET-1 are higher in patients with muscle-invasive bladder cancers, which are associated with higher incidence of metastasis, and that high ET-1 levels are associated with decreased disease-specific survival. Consistent with its proinflammatory activity, we found that tumor-derived ET-1 acts through endothelin-1 receptor A (ETAR) to enhance migration and invasion of both tumor cells and macrophages and induces expression of inflammatory cytokines and proteases. Using human and mouse cancer cells depleted of ET-1 and pharmacologic blockade of ET receptors in lung metastasis models, we found that tumor ET-1 expression and ETAR activity are necessary for metastatic lung colonization and that this process is preceded by and dependent on macrophage infiltration of the lung. In contrast, tumor ET-1 expression and ETAR activity appeared less important in established primary or metastatic tumor growth. These findings strongly suggest that ETAR inhibitors might be more effective as adjuvant therapeutic agents than as initial treatment for advanced primary or metastatic disease.
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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.