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Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Green tea polyphenols increase p53 transcriptional activity and acetylation by suppressing class I histone

Vijay S Thakur1, Karishma Gupta, Sanjay Gupta

  • 1Department of Urology and Nutrition, Case Western Reserve University, Cleveland, OH 44106, USA.

International Journal of Oncology
|May 4, 2012
PubMed

Insights

Green tea polyphenols (GTPs) and EGCG activate the tumor suppressor p53 by inhibiting histone deacetylases (HDACs) in prostate cancer cells. This leads to increased cell cycle arrest and apoptosis, suggesting a therapeutic mechanism.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • The tumor suppressor p53's activity is regulated by post-translational modifications like acetylation.
  • Histone deacetylases (HDACs) remove acetyl groups, counteracting acetylation and influencing gene expression.
  • Prostate cancer cells (LNCaP) provide a model to study p53 regulation.

Purpose of the Study:

  • To investigate the effect of green tea polyphenols (GTPs) and epigallocatechin-3-gallate (EGCG) on p53 acetylation.
  • To determine if GTPs/EGCG inhibit HDACs in prostate cancer cells.
  • To elucidate the downstream effects of GTP/EGCG-induced p53 acetylation on cell cycle and apoptosis.

Main Methods:

  • Treatment of LNCaP cells with varying concentrations and durations of GTPs and EGCG.
  • Assay of class I HDAC (HDAC1, 2, 3, 8) activity.
  • Western blot analysis for p53 acetylation at Lys373 and Lys382, and expression of p21/waf1 and Bax.
  • Cell cycle analysis and apoptosis assays.

Main Results:

  • GTPs and EGCG dose- and time-dependently inhibited class I HDACs in LNCaP cells.
  • Treatment led to increased p53 acetylation at Lys373 and Lys382, with sustained effects.
  • Upregulation of p21/waf1 and Bax expression and enhanced p53 binding to their promoters were observed.
  • Increased G0/G1 cell cycle arrest and apoptosis were induced by GTP/EGCG treatment.

Conclusions:

  • GTPs and EGCG activate p53 acetylation by inhibiting class I HDACs in prostate cancer cells.
  • This mechanism contributes to the anti-cancer effects of green tea components, including cell cycle arrest and apoptosis.
  • The findings highlight a potential therapeutic strategy involving green tea extracts for prostate cancer treatment.

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