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Epigenetic distortion to VDR transcriptional regulation in prostate cancer cells

Prashant K Singh1, Craig L Doig, Vineet K Dhiman

  • 1Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

The Journal of Steroid Biochemistry and Molecular Biology
|October 27, 2012
PubMed

Insights

Prostate cancer cells distort vitamin D receptor (VDR) actions by recruiting co-repressors, leading to gene silencing. This epigenetic shift from transient acetylation to stable DNA methylation impacts VDR target genes.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • The vitamin D receptor (VDR) plays a role in various cellular processes, and its function is often altered in cancer.
  • Understanding VDR's specific mechanisms in prostate cancer is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the gene-specific mechanisms underlying VDR dysfunction in prostate cancer.
  • To compare VDR transcriptional responses in non-malignant versus cancer prostate cells.

Main Methods:

  • Time-resolved transcriptional studies of VDR target genes (IGFBP3, G0S2).
  • Chromatin Immunoprecipitation (ChIP) assays to analyze VDR and co-repressor binding.
  • Comparison of VDR ligand responses in RWPE-1 and PC-3 cell lines.

Main Results:

  • Prostate cancer cells (PC-3) exhibit suppressed VDR transcriptional responses compared to normal cells (RWPE-1).
  • VDR target genes IGFBP3 and G0S2 showed reduced responsiveness in PC-3 cells.
  • VDR-induced enrichment of NCOR1 at target gene promoter regions was observed in PC-3 cells, indicating co-repressor recruitment.

Conclusions:

  • VDR inappropriately recruits co-repressors in prostate cancer cells, leading to gene silencing.
  • This process involves a shift from transient epigenetic modifications (H3K9 acetylation) to stable DNA methylation.
  • Distorted VDR signaling contributes to prostate cancer progression through epigenetic alterations.

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