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An Orthotopic Murine Model of Human Prostate Cancer Metastasis
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Green tea polyphenols causes cell cycle arrest and apoptosis in prostate cancer cells by suppressing class I histone

Vijay S Thakur1, Karishma Gupta, Sanjay Gupta

  • 1Department of Urology, Case Western Reserve University & University Hospitals Case Medical Center, Cleveland, OH 44106, USA.

Carcinogenesis
|November 25, 2011
PubMed

Insights

Green tea polyphenols (GTPs) inhibit histone deacetylase (HDAC) activity, leading to cell cycle arrest and apoptosis in prostate cancer cells. This suggests GTPs offer a novel therapeutic strategy for prostate cancer via HDAC inhibition.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Green tea polyphenols (GTPs) show potential in cancer treatment by reactivating silenced genes.
  • The precise molecular mechanisms of GTPs' antiproliferative effects, particularly their relation to histone deacetylase (HDAC) inhibition, require further elucidation.

Purpose of the Study:

  • To investigate the molecular mechanisms behind the antiproliferative effects of GTPs in human prostate cancer cells.
  • To determine if GTPs function similarly to HDAC inhibitors and explore their impact on gene expression and cell cycle regulation.

Main Methods:

  • Human prostate cancer cell lines (LNCaP and PC-3) were treated with varying concentrations of GTPs.
  • Histone deacetylase (HDAC) activity, protein expression, and histone acetylation levels were assessed.
  • Expression of p21/waf1 and Bax, cell cycle distribution, and apoptosis were analyzed.
  • The role of the proteasome in GTP-induced HDAC modulation was investigated using MG132.

Main Results:

  • GTP treatment dose-dependently inhibited class I HDAC activity and protein expression in both cell lines.
  • GTPs increased histone H3 acetylation, enhancing accessibility to p21/waf1 and Bax promoter regions.
  • Upregulation of p21/waf1 and Bax at protein and message levels was observed.
  • GTP treatment promoted proteasomal degradation of class I HDACs, leading to G(0)-G(1) cell cycle arrest and apoptosis.

Conclusions:

  • GTPs exhibit antiproliferative effects in prostate cancer cells by inhibiting HDACs and inducing proteasomal degradation of these enzymes.
  • These mechanisms are independent of p53 status, highlighting GTPs as a potential therapeutic agent for prostate cancer.
  • GTPs represent a novel approach for prostate cancer prevention and therapy through HDAC inhibition.

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