ArticleOncogene2001
p73 Overexpression increases VEGF and reduces thrombospondin-1 production: implications for tumor angiogenesis.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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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
19 citing papers in PubMed, 52 citations in OpenAlex.
- NOL7 Inhibits Ovarian Cancer Progression and Suppresses Angiogenesis by Stabilizing GADD45A to Deactivate STAT3.Cancer science · 2026Article
- Review
- Peptidome characterization of ovarian cancer serum and the identification of tumor suppressive peptide ZYXAnnals of translational medicine · 2020Article
- Association between TAp73, p53 and VASH1 expression in lung adenocarcinoma.Oncology letters · 2018Article
- Prediction of chemo-response in serous ovarian cancer.Molecular cancer · 2016Article
- p73: a Positive or Negative Regulator of Angiogenesis, or Both?Molecular and cellular biology · 2015Review
- Novel endogenous angiogenesis inhibitors and their therapeutic potential.Acta pharmacologica Sinica · 2015Review
- p73 is required for endothelial cell differentiation, migration and the formation of vascular networks regulating VEGF and TGFβ signaling.Cell death and differentiation · 2015Article
- Hypoxia-inducible TAp73 supports tumorigenesis by regulating the angiogenic transcriptome.Nature cell biology · 2015Article
- TAp73 opposes tumor angiogenesis by promoting hypoxia-inducible factor 1α degradation.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Non-small cell lung cancer is susceptible to induction of DNA damage responses and inhibition of angiogenesis by telomere overhang oligonucleotides.Cancer letters · 2014Article
- The p53 family and VEGF regulation: "It's complicated".Cell cycle (Georgetown, Tex.) · 2013Article
- Gene expression profiles can predict panitumumab monotherapy responsiveness in human tumor xenograft models.Neoplasia (New York, N.Y.) · 2013Article
- Tumor angiogenesis as a target for dietary cancer prevention.Journal of oncology · 2012Article
- Mining the ovarian cancer ascites proteome for potential ovarian cancer biomarkers.Molecular & cellular proteomics : MCP · 2009Article
- Thrombospondin and apoptosis: molecular mechanisms and use for design of complementation treatments.Current drug targets · 2008Review
- A homeobox gene related to Drosophila distal-less promotes ovarian tumorigenicity by inducing expression of vascular endothelial growth factor and fibroblast growth factor-2.The American journal of pathology · 2007Article
- Article
- Generation of a syngeneic mouse model to study the effects of vascular endothelial growth factor in ovarian carcinoma.The American journal of pathology · 2002Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor neovascularization is controlled by a balance between positive and negative effectors, whose production can be regulated by oncogenes and tumor suppressor genes. The aim of this study was to investigate whether the angiogenic potential of tumors could also be controlled by p73, a gene homologous to the tumor suppressor p53, whose involvement in tumor angiogenesis is known. We have studied the production of proangiogenic (VEGF, FGF-2, PIGF and PDGF) and antiangiogenic (TSP-1) factors in two p73 overexpressing clones obtained from the human ovarian carcinoma cells A2780. TSP-1 was downregulated in both clones compared to mock transfected cells, both at mRNA and protein level. Conversely, both clones showed an increased production of VEGF mRNA and protein. For both TSP-1 and VEGF, regulation of expression was partially due to modulation of the promoter activity, and was dependent on p53 status. Production of the other angiogenic factors FGF-2, PIGF and PDGF-B was also increased in p73 overexpressing clones. The two clones were more angiogenic than parental cells, as shown in vitro by their increased chemotactic activity for endothelial cells, and in vivo by the generation of more vascularized tumors. These findings suggest a potential role of p73 in tumor angiogenesis.
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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.