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DNA methylation and histone modifications of Wnt genes by genistein during colon cancer development

Yukun Zhang1, Qian Li, Hong Chen

  • 1Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.

Carcinogenesis
|April 20, 2013
PubMed

Insights

Dietary genistein (GEN) and soy protein isolate (SPI) use epigenetic modifications to suppress WNT gene expression, reducing colon cancer development. These compounds alter DNA methylation and histone modifications, controlling WNT gene responses to carcinogens.

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Cancer Research

Background:

  • WNT signaling is crucial in colon cancer development.
  • Soy protein isolate (SPI) and genistein (GEN) have shown potential in repressing WNT signaling and reducing pre-neoplastic lesions.
  • Azoxymethane (AOM) is a chemical carcinogen used to induce colon cancer in experimental models.

Purpose of the Study:

  • To elucidate the epigenetic mechanisms by which genistein (GEN) regulates WNT gene expression during colon cancer development.
  • To investigate the role of SPI and GEN in inducing epigenetic modifications on Sfrp2, Sfrp5, and Wnt5a genes.
  • To understand how these epigenetic changes suppress WNT gene expression induced by azoxymethane (AOM).

Main Methods:

  • Assessing histone H3 acetylation (H3Ac) and RNA polymerase II binding at gene promoter regions.
  • Quantifying nuclear histone deacetylase 3 levels.
  • Measuring histone trimethylation (H3K9Me3) and phosphorylation (H3S10P).
  • Analyzing gene methylation using bisulfite sequencing.
  • Correlating epigenetic modifications with gene expression levels.

Main Results:

  • SPI and GEN downregulated H3Ac and RNA polymerase II binding at Sfrp2, Sfrp5, and Wnt5a promoters.
  • SPI and GEN increased nuclear histone deacetylase 3 levels.
  • Diets suppressed H3K9Me3 and H3S10P.
  • Gene methylation increased, inversely correlating with reduced gene expression.
  • Dietary GEN induced DNA methylation at the Sfrp5 promoter CpG island.

Conclusions:

  • Dietary genistein (GEN) employs a multi-faceted epigenetic mechanism involving DNA methylation and histone modifications to control WNT gene expression during carcinogen induction.
  • These epigenetic alterations at regulatory regions suppress WNT gene responses, potentially contributing to colon cancer prevention.
  • The findings highlight the interplay between DNA methylation and histone modifications in mediating the effects of dietary compounds on carcinogenesis.

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