Modulation of the Vitamin D3 Response by Cancer-Associated Mutant p53 Journal Articles uri icon

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  • 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.


  • Stambolsky, Perry
  • Tabach, Yuval
  • Fontemaggi, Giulia
  • Weisz, Lilach
  • Maor-Aloni, Revital
  • Sigfried, Zahava
  • Shiff, Idit
  • Kogan, Ira
  • Shay, Moshe
  • Kalo, Eyal
  • Blandino, Giovanni
  • Simon, Itamar
  • Oren, Moshe
  • Rotter, Varda

publication date

  • March 2010