ArticleProstate cancer and prostatic diseases2008
Neutral endopeptidase inhibits prostate cancer tumorigenesis by reducing FGF-2-mediated angiogenesis.
Article in Prostate cancer and prostatic diseases, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02065323 (A Randomized Open-label Phase II Study of Oral Dovitinib in Combination With Androgen Deprivation Therapy to Delay the Onset of Castration-resistant Disease in Patients With Metastatic Prostate Cancer Undergoing Primary Androgen Deprivation Therapy), which is not on this map. Cited by 8 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.
The trial behind it
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.
A Randomized Open-label Phase II Study of Oral Dovitinib in Combination With Androgen Deprivation Therapy to Delay the Onset of Castration-resistant Disease in Patients With Metastatic Prostate Cancer Undergoing Primary Androgen Deprivation Therapy
Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- A function-blocking CD47 antibody modulates extracellular vesicle-mediated intercellular signaling between breast carcinoma cells and endothelial cells.Journal of cell communication and signaling · 2018Article
- Long-term neprilysin inhibition - implications for ARNIs.Nature reviews. Cardiology · 2017Review
- Substance P and thiorphan synergically enhance angiogenesis in wound healing.Tissue engineering and regenerative medicine · 2016Article
- Epigenetic suppression of neprilysin regulates breast cancer invasion.Oncogenesis · 2016Article
- Role of B Cell Development Marker CD10 in Cancer Progression and Prognosis.Molecular biology international · 2016Review
- Neprilysin regulates pulmonary artery smooth muscle cell phenotype through a platelet-derived growth factor receptor-dependent mechanism.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Synergistic relationship between dipeptidyl peptidase IV and neutral endopeptidase expression and the combined prognostic significance in osteosarcoma patients.Medical oncology (Northwood, London, England) · 2013Article
- Adenoviral neutral endopeptidase gene delivery in combination with paclitaxel for the treatment of prostate cancer.International journal of oncology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Neutral endopeptidase (NEP) is a cell surface peptidase that catalytically inactivates a variety of physiologically active peptides including basic fibroblast growth factor (FGF-2). We investigated the effect of using lentivirus to overexpress NEP in NEP-deficient DU145 prostate cancer cells. Third-generation lentiviral vectors encoding wild-type NEP (L-NEP), catalytically inactive mutant NEP (L-NEPmu), and green fluorescent protein (L-GFP) were stably introduced into DU145 cells. FGF-2 levels in cell culture supernatants decreased by 80% in L-NEP-infected DU145 cells compared to cells infected with L-NEPmu or L-GFP (P<0.05) while levels of other angiogenic factors were not altered. In vitro tubulogenesis of human vascular endothelial cells induced by conditioned media from DU145 cells infected with L-NEP was significantly reduced compared with that from DU145 cells infected with L-GFP (P<0.05). Tumor xenografts from L-NEP-infected DU145 cells were significantly smaller compared to control cell xenografts and vascularity within these tumors was decreased (P<0.05). Our data suggest that stable expression of NEP in DU145 cells inhibits prostate cancer tumorigenicity by inhibiting angiogenesis, with a probable mechanism being proteolytic inactivation of FGF-2.
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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.