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Epigenetic modifications of the Estrogen receptor beta gene in epithelial ovarian cancer cells

Oi Wah Stephanie Yap1, Ganapathy Bhat, Liang Liu

  • 1Department of Obstetrics and Gynecology, Morehouse School of Medicine, Atlanta, GA 30310, USA.

Anticancer Research
|April 1, 2009
PubMed
Abstract

Insights

Epigenetic modifications like DNA methylation influence estrogen receptor expression in ovarian cancer. Inhibiting DNA methyltransferase (DNMT) and histone deacetylase (HDAC) suppressed tumor growth.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Estrogen insensitivity in ovarian cancer remains poorly understood.
  • Epigenetic mechanisms, particularly DNA methylation, are implicated in silencing estrogen receptor (ER) gene expression.

Purpose of the Study:

  • To investigate the role of epigenetic modifications in estrogen receptor beta (ERbeta) regulation in ovarian cancer.
  • To determine the effects of epigenetic inhibitors on ovarian cancer cell growth and gene expression.

Main Methods:

  • Ovarian cancer cell lines (SKOV3, HEY) were treated with DNA methyltransferase (DNMT) inhibitor (5-aza-2'-deoxycytidine, AzaC) and histone deacetylase (HDAC) inhibitor (trichostatin, TSA).
  • ERbeta promoter methylation was analyzed using bisulfite sequencing.
  • Gene expression changes were assessed via oligonucleotide array studies.

Main Results:

  • Differential ERbeta promoter methylation was observed between SKOV3 and HEY cells, with SKOV3 showing relative hypomethylation.
  • AzaC and TSA treatments led to specific CpG demethylation and significant inhibition of ovarian cancer cell growth.
  • Numerous gene expression alterations were detected following treatment with AzaC and TSA.

Conclusions:

  • The ERbeta promoter exhibits differential methylation patterns in ovarian cancer cells.
  • Epigenetic modulation using AzaC and TSA demonstrates potential for inhibiting ovarian cancer cell proliferation.

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