期刊
CANCER CELL
卷 17, 期 3, 页码 273-285出版社
CELL PRESS
DOI: 10.1016/j.ccr.2009.11.025
关键词
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资金
- European Community [502983]
- Flight Attendant Medical Research Institute [R37 CA40099]
- National Cancer Institute
- Dr. Miriam and Sheldon Adelson Medical Research Foundation
- Yad Abraham Center for Cancer Diagnosis and Therapy
The p53 gene is mutated in many human tumors. Cells of such tumors often contain abundant mutant p53 (mutp53) protein, which may contribute actively to tumor progression via a gain-of-function mechanism. We applied ChIP-on-chip analysis and identified the vitamin D receptor (VDR) response element as overrepresented in promoter sequences bound by mutp53. We report that mutp53 can interact functionally and physically with VDR. Mutp53 is recruited to VDR-regulated genes and modulates their expression, augmenting the transactivation of some genes and relieving the repression of others. Furthermore, mutp53 increases the nuclear accumulation of VDR. Importantly, mutp53 converts vitamin D into an antiapoptotic agent. Thus, p53 status can determine the biological impact of vitamin D on tumor cells.
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