Key result
SR 25989 upregulated thrombospondin-1 expression and increased p53 protein levels in human vascular endothelial cells and fibroblasts, correlating with decreased cell density.
Why the study?
Does SR 25989 upregulate thrombospondin-1 expression in human vascular endothelial cells and foreskin fibroblasts?
Population
Human vascular endothelial cells and human foreskin fibroblasts
Design
Preclinical
Authors
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Should not change practice; leaves open SR 25989's role in angiogenesis modulation.
Does SR 25989 upregulate thrombospondin-1 expression in human vascular endothelial cells and foreskin fibroblasts?
SR 25989 upregulates thrombospondin-1 and p53 in human endothelial cells and fibroblasts, suggesting potential as an adjuvant anti-angiogenic therapy in cancer.
C Klein-Soyer (1997) studied this question. SR 25989 was evaluated on Regulation of proteins involved in matrix remodeling (thrombospondin-1, p53). SR 25989 upregulated thrombospondin-1 expression and increased p53 protein levels in human vascular endothelial cells and fibroblasts, correlating with decreased cell density.
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