Published in

Cell Press, Cancer Cell, 5(17), p. 523, 2010

DOI: 10.1016/j.ccr.2010.04.017

Cell Press, Cancer Cell, 3(17), p. 273-285, 2010

DOI: 10.1016/j.ccr.2009.11.025

Links

Tools

Export citation

Search in Google Scholar

Modulation of the Vitamin D3 response by cancer-associated mutant p53

Journal article published in 2010 by Perry Stambolsky, Yuval Tabach, Giulia Fontemaggi ORCID, Lilach Weisz, Revital Maor-Aloni, Zehava Siegfried, Zahava Sigfried, Idit Shiff, Ira Kogan, Moshe Shay, Eyal Kalo, Giovanni Blandino, Itamar Simon, Moshe Oren, Varda Rotter
This paper is available in a repository.
This paper is available in a repository.

Full text: Download

Green circle
Preprint: archiving allowed
Upload
Orange circle
Postprint: archiving restricted
Upload
Red circle
Published version: archiving forbidden
Policy details
Data provided by SHERPA/RoMEO

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 (GOF) mechanism. We applied ChIP-on-chip analysis and identified the VDR (vitamin D receptor) response element as over-represented 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.