Evidence map›Paper›PMID 22006862›Full record

ArticleMolecular carcinogenesis2012

Plant flavone apigenin inhibits HDAC and remodels chromatin to induce growth arrest and apoptosis in human prostate cancer cells: in vitro and in vivo study.

Mitali Pandey, Parminder Kaur, Sanjeev Shukla, Ata Abbas, Pingfu Fu, Sanjay Gupta

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 4 pooled it
2.9field-weighted citation impact, top 9% 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

100 citing papers in PubMed, 4 syntheses or guidelines pooled it, 214 citations in OpenAlex.

  1. Pooled it
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  4. Dietary polyphenols in prevention and treatment of prostate cancer.International journal of molecular sciences · 2015
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  10. Food science & nutrition · 2026
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40 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Mitali PandeyDepartment of Urology, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Parminder Kaur
Sanjeev Shukla
Ata Abbas
Pingfu Fu
Sanjay Gupta
Case Western Reserve University · USUniversity Hospitals Case Medical Center · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
Prostate Cancer Chemoprevention by ApigeninR01CA108512 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI GUPTA, SANJAY · 2004 to 2014
$2.4M
Chamomile as Medicine for Prostate cancerR01AT002709 · NCCIH · CASE WESTERN RESERVE UNIVERSITY · PI GUPTA, SANJAY · 2005 to 2009
$1.3M
NCCIH NIH HHS R01 AT002709NCI NIH HHS P30 CA043703NCI NIH HHS P30 CA43703NCI NIH HHS R01 CA108512
6 · The paper itself

Abstract

Apigenin (4',5,7,-trihydroxyflavone), an anticancer agent, selectively toxic to cancer cells induces cell cycle arrest and apoptosis through mechanisms that have not been fully elucidated. Our studies indicate that apigenin-mediated growth inhibitory responses are due to inhibition of class I histone deacetylases (HDACs) in prostate cancer cells. Treatment of PC-3 and 22Rv1 cells with apigenin (20-40 µM) resulted in the inhibition of HDAC enzyme activity, specifically HDAC1 and HDAC3 at the protein and message level. Apigenin-mediated HDAC inhibition resulted in global histone H3 and H4 acetylation, as well as localized hyperacetylation of histone H3 on the p21/waf1 promoter. A corresponding increase was observed in p21/waf1 and bax protein and mRNA expression after apigenin exposure, consistent with the use of HDAC inhibitor, trichostatin A. The downstream events demonstrated cell cycle arrest and induction of apoptosis in both cancer cells. Studies of PC-3 xenografts in athymic nude mice further demonstrated that oral intake of apigenin at doses of 20 and 50 µg/mouse/d over an 8-wk period resulted in a marked reduction in tumor growth, HDAC activity, and HDAC1 and HDAC3 protein expression at both doses of apigenin. An increase in p21/waf1 expression was observed in apigenin-fed mice, compared to the control group. Furthermore, apigenin intake caused a significant decrease in bcl2 expression with concomitant increase in bax, shifting the bax/bcl2 ratio in favor of apoptosis. Our findings confirm for the first time that apigenin inhibits class I HDACs, particularly HDAC1 and HDAC3 and its exposure results in reversal of aberrant epigenetic events that promote malignancy. © 2011 Wiley Periodicals, Inc.

Indexed as

AcetylationAnimalsApigeninApoptosisBase SequenceCell DivisionCell Line, TumorChromatin Assembly and DisassemblyChromatin ImmunoprecipitationCyclin-Dependent Kinase Inhibitor p21DNA PrimersHistone Deacetylase InhibitorsHumansIn Vitro TechniquesMaleMiceApigeninCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA PrimersHistone Deacetylase Inhibitors

Identifiers

PMID22006862
PMCPMC4019962
OpenAlexW2055021348

What OpenQuestion holds

Textmetadata
LicenceTDM
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.