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Cancer Cell. 2010 Mar 16;17(3):273-85. doi: 10.1016/j.ccr.2009.11.025.

Modulation of the vitamin D3 response by cancer-associated mutant p53.

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1
Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel. perrystam@hotmail.com

Erratum in

  • Cancer Cell. 2010 May 18;17(5):523. Sigfried, Zahava [corrected to Siegfried, Zehava].

Abstract

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.

PMID:
20227041
PMCID:
PMC2882298
DOI:
10.1016/j.ccr.2009.11.025
[Indexed for MEDLINE]
Free PMC Article
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