ArticleOncogene1999
The Wilms' tumor gene product represses the transcription of thrombospondin 1 in response to overexpression of c-Jun.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Mechanisms of transcriptional regulation by WT1 (Wilms' tumour 1).The Biochemical journal · 2014Review
- Invoking the power of thrombospondins: regulation of thrombospondins expression.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
- Coronary heart disease-associated variation in TCF21 disrupts a miR-224 binding site and miRNA-mediated regulation.PLoS genetics · 2014Article
- Differentiation of human fetal multipotential neural progenitor cells to astrocytes reveals susceptibility factors for JC virus.Journal of virology · 2013Article
- Disease-related growth factor and embryonic signaling pathways modulate an enhancer of TCF21 expression at the 6q23.2 coronary heart disease locus.PLoS genetics · 2013Article
- p53-responsive miR-194 inhibits thrombospondin-1 and promotes angiogenesis in colon cancers.Cancer research · 2011Article
- Beta1 integrin cytoplasmic variants differentially regulate expression of the antiangiogenic extracellular matrix protein thrombospondin 1.Cancer research · 2009Article
- Antagonistic regulation of cell-matrix adhesion by FosB and DeltaFosB/Delta2DeltaFosB encoded by alternatively spliced forms of fosB transcripts.Molecular biology of the cell · 2008Article
- Thrombospondin and apoptosis: molecular mechanisms and use for design of complementation treatments.Current drug targets · 2008Review
- Disruption of the thrombospondin-2 gene alters the lamellar morphology but does not permit vascularization of the adult mouse lumbar disc.Arthritis research & therapy · 2008Article
- A tumor suppressor and oncogene: the WT1 story.Leukemia · 2007Review
- Article
- NOL7 is a nucleolar candidate tumor suppressor gene in cervical cancer that modulates the angiogenic phenotype.Oncogene · 2006Article
- Hepatocyte growth factor/scatter factor mediates angiogenesis through positive VEGF and negative thrombospondin 1 regulation.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Wnt-4 regulation by the Wilms' tumour suppressor gene, WT1.Oncogene · 2002Article
- p73 Overexpression increases VEGF and reduces thrombospondin-1 production: implications for tumor angiogenesis.Oncogene · 2001Article
- In vivo mechanisms by which tumors producing thrombospondin 1 bypass its inhibitory effects.Genes & development · 2001Article
- Expression of thrombospondin-1 in human hepatocarcinoma cell lines and its regulation by transcription factor Jun/AP-1.Molecular and cellular biochemistry · 2001Article
- Transcriptional control of SPARC by v-Jun and other members of the AP1 family of transcription factors.Oncogene · 2000Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Thrombospondin 1 (TSP1) is known for its significant anti-angiogenic properties. In a previous study, we have shown that transient or stable overexpression of the transcription factor c-Jun, in rat fibroblasts, leads to repression of TSP1. We now demonstrate that the c-Jun-induced repression of TSP1 does not occur directly and does not require binding of c-Jun to the TSP1 promoter. Instead, repression involves a factor secreted by c-Jun-overexpressing cells. This secreted factor triggers a signal transduction pathway from the membrane to the nucleus, and these signals lead to the binding of the product of the Wilms' tumor suppressor gene, WT1, to the -210 region of the TSP1 promoter. This region binds WT1 and SP1, but not EGR1, although its sequence fits the consensus binding site for this transcription factor. WT1 overexpression in transfected cells inhibits endogenous TSP1 gene expression and TSP1 transcription in experiments using TSP1 promoter-reporter constructs. The WT1 - KTS isoform is more active in repressing TSP1 transcription than WT1 + KTS, while EGR1 is inactive. Enhancement of WT1 binding to DNA in response to c-Jun does not require de novo protein synthesis. The above mechanism for TSP1 repression could apply to other genes, thus coordinating their regulation in the vicinity of a c-Jun-overexpressing cell. We conclude that WT1, which was discovered as a result of its tumor suppressor properties, may also possess oncogenic characteristics in the c-Jun transformation process, and thus repress the anti-angiogenic protein, TSP1.
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