ArticleBritish journal of cancer2008
Isoforms of endothelin-converting enzyme-1 (ECE-1) have opposing effects on prostate cancer cell invasion.
Article in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Humoral Immune Response against Nontargeted Tumor Antigens after Treatment with Sipuleucel-T and Its Association with Improved Clinical Outcome.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Trial
- ECE1c promotes glioblastoma invasion via the ROCK2-MYH10 axis and interaction with ACTB.American journal of translational research · 2026Article
- Decreased Endothelin-1 bioavailability impairs aggressiveness of gallbladder cancer cells.Biological research · 2025Article
- Cisplatin-resistance and aggressiveness are enhanced by a highly stable endothelin-converting enzyme-1c in lung cancer cells.Biological research · 2024Article
- Heterogeneous genetic architectures of prostate cancer susceptibility in sub-Saharan Africa.Nature genetics · 2024Article
- Heterogeneous genetic architectures and evolutionary genomics of prostate cancer in Sub-Saharan Africa.Research square · 2023Article
- Article
- Endothelin-converting enzyme-1c promotes stem cell traits and aggressiveness in colorectal cancer cells.Molecular oncology · 2020Article
- Phosphorylation of Endothelin-Converting Enzyme-1c at Serines 18 and 20 by CK2 Promotes Aggressiveness Traits in Colorectal Cancer Cells.Frontiers in oncology · 2020Article
- Pharmacological hypothesis: Nitric oxide-induced inhibition of ADAM-17 activity as well as vesicle release can in turn prevent the production of soluble endothelin-converting enzyme.Pharmacology research & perspectives · 2017Review
- The role of epithelial-mesenchymal transition drivers ZEB1 and ZEB2 in mediating docetaxel-resistant prostate cancer.Molecular oncology · 2017Article
- CK2 in Cancer: Cellular and Biochemical Mechanisms and Potential Therapeutic Target.Pharmaceuticals (Basel, Switzerland) · 2017Review
- N-terminal domain of Bothrops asper Myotoxin II Enhances the Activity of Endothelin Converting Enzyme-1 and Neprilysin.Scientific reports · 2016Article
- Colon cancer cell invasion is promoted by protein kinase CK2 through increase of endothelin-converting enzyme-1c protein stability.Oncotarget · 2015Article
- Automated analysis of immunohistochemistry images identifies candidate location biomarkers for cancers.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Endothelins and their receptors in cancer: identification of therapeutic targets.Pharmacological research · 2011Review
- Role of the endothelin axis and its antagonists in the treatment of cancer.British journal of pharmacology · 2011Review
- Endothelin.Cellular and molecular life sciences : CMLS · 2011Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cross-talk between tumour and stromal cells can profoundly influence cancer cell invasion by increasing the availability of mitogenic peptides such as endothelin-1 (ET-1). Endothelin-1 is elevated in men with metastatic prostate cancer (PC), and can exert both an autocrine (epithelial) and a paracrine (stromal) influence on growth. Endothelin-1 is generated from its inactive precursor big-ET-1 by endothelin-converting enzyme 1 (ECE-1). We and others have demonstrated that ECE-1 expression is significantly elevated in tumours and surrounding stromal tissue. Our current data show siRNA-mediated knockdown of stromal ECE-1 reduces epithelial (PC-3) cell invasion in coculture. Interestingly, readdition of ET-1 only partially recovers this effect suggesting a novel role for ECE-1 independent of ET-1 activation. Parallel knockdown of ECE-1 in both stromal and epithelial compartments results in an additive decrease in cell invasion. We extrapolated this observation to the four recognised isoforms ECE-1a, ECE-1b, ECE-1c and ECE-1d. Only ECE-1a and ECE-1c were significant but with reciprocal effects on cell invasion. Transient ECE-1c overexpression increased PC-3 invasiveness through matrigel, whereas transient ECE-1a expression suppressed invasion. Furthermore, transient ECE-1a expression in stromal cells strongly counteracts the effect of transient ECE-1c expression in PC-3 cells. The ECE-1 isoforms may, therefore, be relevant targets for antiinvasive therapy in prostate and other cancers.
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