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Promoter de-methylation of cyclin D2 by sulforaphane in prostate cancer cells

Anna Hsu1, Carmen P Wong, Zhen Yu

  • 1School of Biological and Population Health Sciences, 103 Milam Hall, Oregon State University, Corvallis, OR 97331, USA.

Clinical Epigenetics
|February 4, 2012
PubMed

Insights

Sulforaphane (SFN) reduces prostate cancer cell growth by altering DNA methylation. This cruciferous vegetable compound lowers DNA methyltransferases and decreases cyclin D2 promoter methylation, leading to increased cyclin D2 expression.

Area of Science:

  • Epigenetics
  • Molecular Oncology
  • Nutritional Biochemistry

Background:

  • Sulforaphane (SFN), from cruciferous vegetables, exhibits anti-proliferative effects in prostate cancer.
  • SFN's epigenetic modulation, particularly histone deacetylase (HDAC) inhibition, is known, but its impact on DNA methylation is less understood.
  • Cyclin D2 promoter hyper-methylation is linked to prostate cancer progression, and its re-expression inhibits cancer cell proliferation.

Purpose of the Study:

  • To investigate the effects of SFN on the DNA methylation status of the cyclin D2 promoter in LnCap prostate cancer cells.
  • To determine how SFN-induced alterations in cyclin D2 promoter methylation influence cyclin D2 gene expression.
  • To elucidate the epigenetic mechanisms underlying SFN's chemopreventive potential in prostate cancer.

Main Methods:

  • Treatment of LnCap prostate cancer cells with SFN.
  • Assessment of DNA methyltransferase (DNMT) expression levels.
  • Analysis of DNA methylation status in specific regions of the cyclin D2 promoter (c-Myc and Sp1 binding sites).
  • Quantification of cyclin D2 gene and transcript levels.

Main Results:

  • SFN significantly reduced the expression of DNA methyltransferases (DNMTs), specifically DNMT1 and DNMT3b.
  • SFN treatment led to a significant decrease in DNA methylation within the cyclin D2 promoter, particularly at sites with c-Myc and Sp1 binding elements.
  • Reduced cyclin D2 promoter methylation correlated with a significant increase in cyclin D2 transcript levels.

Conclusions:

  • SFN epigenetically modulates cyclin D2 expression in prostate cancer cells.
  • SFN may counteract prostate cancer progression by reversing methylation-induced silencing of the cyclin D2 gene.
  • These findings highlight SFN's potential as a chemopreventive agent through epigenetic regulation of gene expression.

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