Tumor suppressor U19/EAF2 regulates thrombospondin-1 expression via p53

被引：0

作者：

F Su

L E Pascal

W Xiao

Z Wang

机构：

[1] University of Pittsburgh Cancer Institute,Department of Urology

[2] University of Pittsburgh School of Medicine,Department of Pharmacology and Chemical Biology

[3] Key Laboratory of Biodiversity and Conservation of Aquatic Organisms,undefined

[4] Institute of Hydrobiology,undefined

[5] Chinese Academy of Sciences,undefined

[6] University of Pittsburgh School of Medicine,undefined

[7] 4Current address: Center for Nuclear Receptors and Cell Signaling,undefined

[8] University of Houston,undefined

[9] Houston,undefined

[10] TX 77204,undefined

[11] USA.,undefined

来源：

Oncogene | 2010年 / 29卷

关键词：

U19/EAF2; prostate cancer; tumor suppressor; TSP-1; p53;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

Inactivation of U19/EAF2 has been shown previously to lead to tumorigenesis in multiple organs; however, the mechanism of U19/EAF2 tumor suppression remains unclear. In this paper, we report that the expression of an anti-angiogenic protein, thrombospondin-1 (TSP-1) is down-regulated in the prostate and liver of U19/EAF2 knockout mouse. The U19/EAF2 knockout liver displayed increased CD31-positive blood vessels, suggesting that the TSP-1 down-regulation can contribute to increased angiogenesis. TSP-1 is reported to be a p53-target gene and p53 is a known binding partner of ELL, which binds to U19/EAF2. Here, we show that U19/EAF2 can co-localize and co-immunoprecipitate with p53 in transfected cells. In a TSP-1 promoter-driven luciferase reporter assay, p53 transfection suppressed the TSP-1 promoter activity and U19/EAF2 co-transfection blocked the p53 suppression of TSP-1 promoter. However, U19/EAF2 transfection alone had little or no effect on the TSP-1 promoter. The above observations together suggest that U19/EAF2 regulates the expression of TSP-1 via blocking p53 repression of the TSP-1 promoter.

引用

页码：421 / 431

页数：10

共 149 条

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