ArticleCancer research2008
Endothelial function of von Hippel-Lindau tumor suppressor gene: control of fibroblast growth factor receptor signaling.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 30 citations in OpenAlex.
- Fibroblast growth factor receptor expression in hemangioblastomas: A novel therapeutic target.PloS one · 2025Article
- Review
- Loss of Function of von Hippel-Lindau Trigger Lipocalin 2-Dependent Inflammatory Responses in Cultured and Primary Renal Tubular Cells.Oxidative medicine and cellular longevity · 2021Article
- Intraoral Excision and Preoperative Embolization of a Von Hippel-Lindau Disease-associated Facial Arteriovenous Malformation.Plastic and reconstructive surgery. Global open · 2020Article
- Interaction between Nm23 and the tumor suppressor VHL.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Effects of membrane trafficking on signaling by receptor tyrosine kinases.Cold Spring Harbor perspectives in biology · 2013Review
- Tie2-dependent VHL knockdown promotes airway microvascular regeneration and attenuates invasive growth of Aspergillus fumigatus.Journal of molecular medicine (Berlin, Germany) · 2013Article
- Von Hippel-Lindau disease (VHL): a need for a murine model with retinal hemangioblastoma.Histology and histopathology · 2012Review
- Hypoxia negatively regulates heparan sulfatase 2 expression in renal cancer cell lines.Molecular carcinogenesis · 2012Article
- Systemic VHL gene functions and the VHL disease.FEBS letters · 2012Review
- Complex cellular functions of the von Hippel-Lindau tumor suppressor gene: insights from model organisms.Oncogene · 2012Review
- New insights into the biology of renal cell carcinoma.Hematology/oncology clinics of North America · 2011Review
- HSulf-1 modulates FGF2- and hypoxia-mediated migration and invasion of breast cancer cells.Cancer research · 2011Article
- Drosophila von Hippel-Lindau tumor suppressor gene function in epithelial tubule morphogenesis.Molecular and cellular biology · 2010Article
- Drosophila VHL tumor-suppressor gene regulates epithelial morphogenesis by promoting microtubule and aPKC stability.Development (Cambridge, England) · 2010Article
- Inherited determinants of ovarian cancer survival.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Article
- The role of ets factors in tumor angiogenesis.Journal of oncology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
von Hippel-Lindau (VHL) disease results from germline and somatic mutations in the VHL tumor suppressor gene and is characterized by highly vascularized tumors. VHL mutations lead to stabilization of hypoxia-inducible factor (HIF), which up-regulates proangiogenic factors such as vascular endothelial growth factor (VEGF). This pathway is therefore believed to underlie the hypervascular phenotypes of the VHL tumors. However, recent studies have identified novel VHL functions that are independent of the HIF-VEGF pathway. In addition, a potential role of VHL in the tumor microenvironment, which carries heterozygous VHL mutations in VHL patients, has been overlooked. Here, we report a novel HIF-independent VHL function in the endothelium. VHL knockdown in primary human microvascular endothelial cells caused defective turnover of surface fibroblast growth factor (FGF) receptor, increased extracellular signal-regulated kinase signaling, and ETS1 activation, leading to increased cell motility in response to FGF and three-dimensional cord formation in vitro. HIF-alpha knockdown in VHL loss-of-function endothelial cells does not impede their elevated in vitro angiogenic activity. Importantly, the elevated angiogenic response to FGF is recapitulated in Vhl-heterozygous mice. Thus, partial loss of function of VHL in endothelium may be a contributing factor in tumor angiogenesis through a HIF-VEGF-independent mechanism.
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What OpenQuestion holds
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.