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Epigenetic control of a VDR-governed feed-forward loop that regulates p21(waf1/cip1) expression and function in

James L Thorne1, Orla Maguire, Craig L Doig

  • 1Institute of Biomedical Research, University of Birmingham, Edgbaston B15 2TT, UK. Moray.Campbell@RoswellPark.org

Nucleic Acids Research
|November 20, 2010
PubMed

Insights

Vitamin D Receptor (VDR) signaling in prostate cells triggers cell cycle arrest by regulating CDKN1A. VDR utilizes specific histone modifications and microRNA co-regulation to control gene expression and cell division.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Epigenetics

Background:

  • The nuclear receptor Vitamin D Receptor (VDR) plays a role in cell cycle regulation.
  • Understanding VDR's mechanism in non-malignant prostate cells is crucial for cancer research.

Purpose of the Study:

  • To elucidate the epigenetic mechanisms by which VDR controls cell cycle arrest in prostate epithelial cells.
  • To investigate the role of histone modifications and microRNA in VDR-mediated CDKN1A regulation.

Main Methods:

  • Analysis of VDR binding sites on the CDKN1A promoter.
  • Assessment of dynamic histone modifications (H3K9ac, H3K27me3) across cell cycle phases.
  • Investigation of VDR's effect on MCM7 gene expression and miR-106b generation.
  • Study of VDR interaction with p53.

Main Results:

  • VDR dynamically induces cell cycle-specific histone modification patterns at CDKN1A promoter sites.
  • Epigenetic events facilitate VDR and p53 cooperation for enhanced p21((waf1/cip1)) activation.
  • VDR binding to MCM7 upregulates miR-106b, influencing p21((waf1/cip1)) expression.

Conclusions:

  • VDR-regulated feed-forward loop involving promoter-specific histone modifications and miRNA co-regulation controls p21((waf1/cip1)) expression and cell cycle arrest.
  • This mechanism in non-malignant cells provides insights into VDR sensitivity and potential resistance in prostate cancer.

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