ArticleJournal of cellular biochemistry2012
Glucose-activated RUNX2 phosphorylation promotes endothelial cell proliferation and an angiogenic phenotype.
Article in Journal of cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Defining the vascular niche of human adipose tissue across metabolic states.Nature metabolism · 2026Article
- Defining the vascular niche of human adipose tissue across metabolic states.bioRxiv : the preprint server for biology · 2025Article
- RUNX transcription factors: biological functions and implications in cancer.Clinical and experimental medicine · 2024Review
- RUNX2 and Cancer.International journal of molecular sciences · 2023Review
- Review
- Stimulation of the Runx2 P1 promoter by collagen-derived dipeptide prolyl-hydroxyproline bound to Foxg1 and Foxo1 in osteoblasts.Bioscience reports · 2021Article
- Delayed tooth movement in Runx2Bone reports · 2020Article
- miR‑204 inhibits the osteogenic differentiation of mesenchymal stem cells by targeting bone morphogenetic protein 2.Molecular medicine reports · 2020Article
- Antitumor efficacy of the Runx2-dendritic cell vaccine in triple-negative breast cancerOncology letters · 2018Article
- Cell-Matrix Interactions and Matricrine Signaling in the Pathogenesis of Vascular Calcification.Frontiers in cardiovascular medicine · 2018Review
- Characterization of CADD522, a small molecule that inhibits RUNX2-DNA binding and exhibits antitumor activity.Oncotarget · 2017Article
- The transcription factor RUNX2 regulates receptor tyrosine kinase expression in melanoma.Oncotarget · 2016Article
- The RUNX2 Transcription Factor Negatively Regulates SIRT6 Expression to Alter Glucose Metabolism in Breast Cancer Cells.Journal of cellular biochemistry · 2015Article
- RUNX2 and the PI3K/AKT axis reciprocal activation as a driving force for tumor progression.Molecular cancer · 2015Review
- Hyperglycemia and redox status regulate RUNX2 DNA-binding and an angiogenic phenotype in endothelial cells.Microvascular research · 2015Article
- A thin layer angiogenesis assay: a modified basement matrix assay for assessment of endothelial cell differentiation.BMC cell biology · 2014Article
- RUNX2 is overexpressed in melanoma cells and mediates their migration and invasion.Cancer letters · 2014Article
- NEU1 sialidase regulates the sialylation state of CD31 and disrupts CD31-driven capillary-like tube formation in human lung microvascular endothelia.The Journal of biological chemistry · 2014Article
- Runx2 activates PI3K/Akt signaling via mTORC2 regulation in invasive breast cancer cells.Breast cancer research : BCR · 2014Article
- Runx2 isoform I controls a panel of proinvasive genes driving aggressiveness of papillary thyroid carcinomas.The Journal of clinical endocrinology and metabolism · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The runt-related protein-2 (RUNX2) is a DNA-binding transcription factor that regulates bone formation, tumor cell metastasis, endothelial cell (EC) proliferation, and angiogenesis. RUNX2 DNA binding is glucose and cell cycle regulated. We propose that glucose may activate RUNX2 through changes in post-translational phosphorylation that are cell cycle-specific and will regulate EC function. Glucose increased cell cycle progression in EC through both G2/M and G1 phases with entry into S-phase occurring only in subconfluent cells. In the absence of nutrients and growth factors (starvation), subconfluent EC were delayed in G1 when RUNX2 expression was reduced. RUNX2 phosphorylation, activation of DNA binding, and pRb phosphorylation were stimulated by glucose and were necessary to promote cell cycle progression. Glucose increased RUNX2 localization at focal subnuclear sites, which co-incided with RUNX2 occupancy of the cyclin-dependent kinase (cdk) inhibitor p21(Cip1) promoter, a gene normally repressed by RUNX2. Mutation of the RUNX2 cdk phosphorylation site in the C-terminal domain (S451A.RUNX2) reduced RUNX2 phosphorylation and DNA binding. Expression of this cdk site mutant in EC inhibited glucose-stimulated differentiation (in vitro tube formation), monolayer wound healing, and proliferation. These results define a novel relationship between glucose-activated RUNX2 phosphorylation, cell cycle progression, and EC differentiation. These data suggest that inhibition of RUNX2 expression or DNA binding may be a useful strategy to inhibit EC proliferation 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.