ArticlePloS one2011
VEGF promotes the transcription of the human PRL-3 gene in HUVEC through transcription factor MEF2C.
Article in PloS one, 2011. 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, 32 citations in OpenAlex.
- Polysialic acid regulates glomerular microvasculature formation by interaction with VEGF-A188 in mice.Angiogenesis · 2025Article
- PRL3-zumab as an anti-angiogenic therapy in neovascular eye diseases.Nature communications · 2025Article
- The PACT Network: PRL, ARL, CNNM, and TRPM Proteins in Magnesium Transport and Disease.International journal of molecular sciences · 2025Review
- Protein Tyrosine Phosphatase PRL-3: A Key Player in Cancer Signaling.Biomolecules · 2024Review
- PRL3 as a therapeutic target for novel cancer immunotherapy in multiple cancer types.Theranostics · 2023Review
- Increased phosphatase regenerating liver-1 trigger vascular remodeling in injured ovary via platelet-derived growth factor signaling pathway.Stem cell research & therapy · 2022Article
- MEF2C shapes the microtranscriptome during differentiation of skeletal muscles.Scientific reports · 2021Article
- Targeting ovarian cancer and endothelium with an allosteric PTP4A3 phosphatase inhibitor.Oncotarget · 2018Article
- Morphology regulation in vascular endothelial cells.Inflammation and regeneration · 2018Review
- Article
- Antibody Array Revealed PRL-3 Affects Protein Phosphorylation and Cytokine Secretion.PloS one · 2017Article
- Regulatory mechanisms of phosphatase of regenerating liver (PRL)-3.Biochemical Society transactions · 2016Review
- Myocyte enhancer factor 2C regulation of hepatocellular carcinoma via vascular endothelial growth factor and Wnt/β-catenin signaling.Oncogene · 2015Article
- Transcription factor MEF2C suppresses endothelial cell inflammation via regulation of NF-κB and KLF2.Journal of cellular physiology · 2015Article
- Phosphatase of regenerating liver: a novel target for cancer therapy.Expert opinion on therapeutic targets · 2014Review
- Protein-tyrosine phosphatase 4A3 (PTP4A3) promotes vascular endothelial growth factor signaling and enables endothelial cell motility.The Journal of biological chemistry · 2014Article
- Article
- A novel chromone derivative with anti-inflammatory property via inhibition of ROS-dependent activation of TRAF6-ASK1-p38 pathway.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphatase of regenerating liver 3 (PRL-3) is known to be overexpressed in many tumors, and its transcript level is high in the vasculature and endothelial cells of malignant tumor tissue. However, the mechanism(s) underlying its enhanced expression and its function in endothelial cells remain unknown. Here, we report that vascular endothelial growth factor (VEGF) can induce PRL-3 transcription in human umbilical vein endothelial cells (HUVEC). An analysis of its 5'UTR revealed that PRL-3 transcription is initiated from two distinct sites, which results in the formation of the two transcripts, PRL-3-iso1 and PRL-3-iso2, but only the latter is up-regulated in HUVEC by VEGF. The PRL-3-iso2 promoter region includes two functional MEF2 (myocyte enhancer factor2) binding sites. The over-expression of the constitutively active form of MEF2C promotes the abundance of the PRL-3-iso2 transcript in a number of human cell lines. The siRNA-induced knockdown of MEF2C abolished the stimulative effect of VEGF on PRL-3 transcript in HUVEC, indicating that the VEGF-induced promotion of PRL-3 expression requires the presence of MEF2C. Finally, blocking PRL-3 activity or expression suppresses tube formation by HUVEC. We suggest that PRL-3 functions downstream of the VEGF/MEF2C pathway in endothelial cells and may play an important role in tumor angiogenesis.
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