Evidence map›Paper›PMID 22114073›Full record

ArticleCarcinogenesis2012

Green tea polyphenols causes cell cycle arrest and apoptosis in prostate cancer cells by suppressing class I histone deacetylases.

Vijay S Thakur, Karishma Gupta, Sanjay Gupta

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 151 citations in OpenAlex.

  1. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
    Review
  2. Review
  3. Epigenetic mechanisms differentially regulate blood pressure and renal dysfunction in male and female Npr1 haplotype mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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  17. The Effect of Green and Black Tea Polyphenols onInternational journal of molecular sciences · 2019
    Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Vijay S ThakurDepartment of Urology, Case Western Reserve University & University Hospitals Case Medical Center, Cleveland, OH 44106, USA.
Karishma Gupta
Sanjay Gupta
University Hospitals Cleveland Medical Center · US

Funding

Molecular Mechanisms of GSTP1 Reactivation by Green Tea PolyphenolsR01CA115491 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI GUPTA, SANJAY · 2007 to 2011
$1.3M
Reactivation of GSTP1 Gene by Green Tea PolyphenolsR21CA109424 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI GUPTA, SANJAY · 2004 to 2005
$252k
NCI NIH HHS R01 CA115491NCI NIH HHS R21 CA109424
6 · The paper itself

Abstract

Green tea polyphenols (GTPs) reactivate epigenetically silenced genes in cancer cells and trigger cell cycle arrest and apoptosis; however, the mechanisms whereby these effects occur are not well understood. We investigated the molecular mechanisms underlying the antiproliferative effects of GTP, which may be similar to those of histone deacetylase (HDAC) inhibitors. Exposure of human prostate cancer LNCaP cells (harboring wild-type p53) and PC-3 cells (lacking p53) with 10-80 μg/ml of GTP for 24 h resulted in dose-dependent inhibition of class I HDAC enzyme activity and its protein expression. GTP treatment causes an accumulation of acetylated histone H3 in total cellular chromatin, resulting in increased accessibility to bind with the promoter sequences of p21/waf1 and Bax, consistent with the effects elicited by an HDAC inhibitor, trichostatin A. GTP treatment also resulted in increased expression of p21/waf1 and Bax at the protein and message levels in these cells. Furthermore, treatment of cells with proteasome inhibitor, MG132 together with GTP prevented degradation of class I HDACs, compared with cells treated with GTP alone, indicating increased proteasomal degradation of class I HDACs by GTP. These alterations were consistent with G(0)-G(1) phase cell cycle arrest and induction of apoptosis in both cell lines. Our findings provide new insight into the mechanisms of GTP action in human prostate cancer cells irrespective of their p53 status and suggest a novel approach to prevention and/or therapy of prostate cancer achieved via HDAC inhibition.

Indexed as

TeaAcetylationApoptosisbcl-2-Associated X ProteinCell Cycle CheckpointsCell ProliferationChromatinCyclin-Dependent Kinase Inhibitor p21Down-RegulationHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansHydroxamic AcidsLeupeptinsMalebcl-2-Associated X Proteinbenzyloxycarbonylleucyl-leucyl-leucine aldehydeChromatinCyclin-Dependent Kinase Inhibitor p21Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHydroxamic AcidsLeupeptinsPolyphenolsProteasome Endopeptidase ComplexTeaTP53 protein, humantrichostatin ATumor Suppressor Protein p53

Identifiers

PMID22114073
PMCPMC3499108
OpenAlexW2121774615

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.