| First Author | Su F | Year | 2010 |
| Journal | Oncogene | Volume | 29 |
| Issue | 3 | Pages | 421-31 |
| PubMed ID | 19826414 | Mgi Jnum | J:168188 |
| Mgi Id | MGI:4887321 | Doi | 10.1038/onc.2009.326 |
| Citation | Su F, et al. (2010) Tumor suppressor U19/EAF2 regulates thrombospondin-1 expression via p53. Oncogene 29(3):421-31 |
| abstractText | 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. |
