Evidence map›Paper›PMID 22591439›Full record

ArticleBMC cancer2012

Plant HDAC inhibitor chrysin arrest cell growth and induce p21WAF1 by altering chromatin of STAT response element in A375 cells.

Manika Pal-Bhadra, M Janaki Ramaiah, T Lakshminarayan Reddy, Anita Krishnan, S N C V L Pushpavalli, K Suresh Babu, Ashok K Tiwari, J Madhusudana Rao, Jhillu S Yadav, Utpal Bhadra

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

38 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Deciphering the Role of Oroxylin A in Liver Fibrosis.Drug design, development and therapy · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Drugging the Epigenome: Overcoming Resistance to Targeted and Immunotherapies in Melanoma.JID innovations : skin science from molecules to population health · 2022
    Review
  17. Review
  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

10 authors at 2 institutions in 1 country.

Manika Pal-BhadraDepartment of Chemical Biology, Indian Institute of Chemical Technology, Hyderabad, India. manikapb@gmail.com
M Janaki Ramaiah
T Lakshminarayan Reddy
Anita Krishnan
S N C V L Pushpavalli
K Suresh Babu
Ashok K Tiwari
J Madhusudana Rao
Jhillu S Yadav
Utpal Bhadra
Indian Institute of Chemical Technology · INCentre for Cellular and Molecular Biology · IN

Funding

Wellcome Trust GAP 0065Wellcome Trust GAP 0158
6 · The paper itself

Abstract

backgroundChrysin and its analogues, belongs to flavonoid family and possess potential anti-tumour activity. The aim of this study is to determine the molecular mechanism by which chrysin controls cell growth and induce apoptosis in A375 cells.

methodsEffect of chrysin and its analogues on cell viability and cell cycle analysis was determined by MTT assay and flowcytometry. A series of Western blots was performed to determine the effect of chrysin on important cell cycle regulatory proteins (Cdk2, cyclin D1, p53, p21, p27). The fluorimetry and calorimetry based assays was conducted for characterization of chrysin as HDAC inhibitor. The changes in histone tail modification such as acetylation and methylation was studied after chrysin treatment was estimated by immuno-fluorescence and western blot analysis. The expression of Bcl-xL, survivin and caspase-3 was estimated in chrysin treated cells. The effect of chrysin on p21 promoter activity was studied by luciferase and ChIP assays.

resultsChrysin cause G1 cell cycle arrest and found to inhibit HDAC-2 and HDAC-8. Chrysin treated cells have shown increase in the levels of H3acK14, H4acK12, H4acK16 and decrease in H3me2K9 methylation. The p21 induction by chrysin treatment was found to be independent of p53 status. The chromatin remodelling at p21WAF1 promoter induces p21 activity, increased STAT-1 expression and epigenetic modifications that are responsible for ultimate cell cycle arrest and apoptosis.

conclusionChrysin shows in vitro anti-cancer activity that is correlated with induction of histone hyperacetylation and possible recruitment of STAT-1, 3, 5 proteins at STAT (-692 to -684) region of p21 promoter. Our results also support an unexpected action of chrysin on the chromatin organization of p21WAF1 promoter through histone methylation and hyper-acetylation. It proposes previously unknown sequence specific chromatin modulations in the STAT responsive elements for regulating cell cycle progression negatively via the induction of the CDK inhibitor p21WAF1.

Indexed as

AcetylationApoptosisBase SequenceCell Cycle CheckpointsCell Line, TumorCell NucleusChromosomes, HumanCyclin-Dependent Kinase Inhibitor p21FlavonoidsGene OrderHistone Deacetylase InhibitorsHistonesHumansMethylationPromoter Regions, GeneticProtein Processing, Post-TranslationalchrysinCyclin-Dependent Kinase Inhibitor p21FlavonoidsHistone Deacetylase InhibitorsHistonesSTAT Transcription Factors

Identifiers

PMID22591439
PMCPMC3407000
OpenAlexW2084897539

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.