Evidence map›Paper›PMID 24563225›Full record

ArticleApoptosis : an international journal on programmed cell death2014

Apigenin induces apoptosis by targeting inhibitor of apoptosis proteins and Ku70-Bax interaction in prostate cancer.

Sanjeev Shukla, Pingfu Fu, Sanjay Gupta

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

Article in Apoptosis : an international journal on programmed cell death, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 2 pooled it
6.6field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Dietary polyphenols in prevention and treatment of prostate cancer.International journal of molecular sciences · 2015
    Pooled it
  3. Article
  4. Article
  5. Food science & nutrition · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Potential anticancer effects and toxicity of flavones luteolin and apigeninJournal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. An Update on the Therapeutic Anticancer Potential ofMolecules (Basel, Switzerland) · 2023
    Review
  20. Review
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 2 institutions in 1 country.

Sanjeev ShuklaDepartment of Urology, Case Western Reserve University & The Urology Institute, University Hospitals Case Medical Center, 10900 Euclid Avenue, Cleveland, OH, 44106, USA.
Pingfu Fu
Sanjay Gupta
University Hospitals Case Medical Center · USCase Western Reserve University · US

Funding

Prostate Cancer Chemoprevention by ApigeninR01CA108512 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI GUPTA, SANJAY · 2004 to 2014
$2.4M
Molecular Mechanisms of GSTP1 Reactivation by Green Tea PolyphenolsR01CA115491 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI GUPTA, SANJAY · 2007 to 2011
$1.3M
Chamomile as Medicine for Prostate cancerR01AT002709 · NCCIH · CASE WESTERN RESERVE UNIVERSITY · PI GUPTA, SANJAY · 2005 to 2009
$1.3M
NCCIH NIH HHS R01 AT002709NCCIH NIH HHS R01AT002709NCI NIH HHS R01 CA108512NCI NIH HHS R01CA108512NCI NIH HHS R01 CA115491NCI NIH HHS R03CA1376676
6 · The paper itself

Abstract

Dysfunction of the apoptotic pathway in prostate cancer cells confers apoptosis resistance towards various therapies. A novel strategy to overcome resistance is to directly target the apoptotic pathway in cancer cells. Apigenin, an anticancer agent, selectively toxic to cancer cells induces cell cycle arrest and apoptosis through mechanisms which are not fully explored. In the present study we provide novel insight into the mechanisms of apoptosis induction by apigenin. Treatment of androgen-refractory human prostate cancer PC-3 and DU145 cells with apigenin resulted in dose-dependent suppression of XIAP, c-IAP1, c-IAP2 and survivin protein levels. Apigenin treatment resulted in significant decrease in cell viability and apoptosis induction with the increase of cytochrome C in time-dependent manner. These effects of apigenin were accompanied by decrease in Bcl-xL and Bcl-2 and increase in the active form of Bax protein. The apigenin-mediated increase in Bax was due to dissociation of Bax from Ku70 which is essential for apoptotic activity of Bax. Apigenin treatment resulted in the inhibition of class I histone deacetylases and HDAC1 protein expression, thereby increasing the acetylation of Ku70 and the dissociation of Bax resulting in apoptosis of cancer cells. Furthermore, apigenin significantly reduced HDAC1 occupancy at the XIAP promoter, suggesting that histone deacetylation might be critical for XIAP downregulation. These results suggest that apigenin targets inhibitor of apoptosis proteins and Ku70-Bax interaction in the induction of apoptosis in prostate cancer cells and in athymic nude mouse xenograft model endorsing its in vivo efficacy.

Indexed as

AnimalsAntigens, NuclearAntineoplastic AgentsApigeninApoptosisbcl-2-Associated X ProteinCell Line, TumorDNA-Binding ProteinsHumansKu AutoantigenMaleMiceMice, NudeProstatic NeoplasmsAntigens, NuclearAntineoplastic AgentsApigeninbcl-2-Associated X ProteinDNA-Binding ProteinsKu AutoantigenXrcc6 protein, humanXrcc6 protein, mouse

Identifiers

PMID24563225
PMCPMC3997183
OpenAlexW2015641994

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.