Evidence map›Paper›PMID 17567991›Full record

ArticleGenome research2007

Butyrate mediates decrease of histone acetylation centered on transcription start sites and down-regulation of associated genes.

Alvaro Rada-Iglesias, Stefan Enroth, Adam Ameur, Christoph M Koch, Gayle K Clelland, Patricia Respuela-Alonso, Sarah Wilcox, Oliver M Dovey, Peter D Ellis, Cordelia F Langford and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Genome research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
–field-weighted citation impact
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

72 citing papers in PubMed, 166 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Butyrate SilencesAllergy, asthma & immunology research · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Role of epigenetics in corneal health and disease.Progress in retinal and eye research · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

12 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

13 authors at 2 institutions in 2 countries.

Alvaro Rada-IglesiasDepartment of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, SE-751 05 Sweden. alvaro.rada@genpat.uu.se
Stefan Enroth
Adam Ameur
Christoph M Koch
Gayle K Clelland
Patricia Respuela-Alonso
Sarah Wilcox
Oliver M Dovey
Peter D Ellis
Cordelia F Langford
Ian Dunham
Jan Komorowski
Claes Wadelius
Wellcome Sanger Institute · GBUppsala University · SE

Funding

Detecting Human Functional Sequences with MicroarraysU01HG003168 · NHGRI · SANGER INSTITUTE · PI DUNHAM, IAN · 2003 to 2006
$1.3M
NHGRI NIH HHS 5 U01 HG003168NHGRI NIH HHS U01 HG003168Wellcome Trust
6 · The paper itself

Abstract

Butyrate is a histone deacetylase inhibitor (HDACi) with anti-neoplastic properties, which theoretically reactivates epigenetically silenced genes by increasing global histone acetylation. However, recent studies indicate that a similar number or even more genes are down-regulated than up-regulated by this drug. We treated hepatocarcinoma HepG2 cells with butyrate and characterized the levels of acetylation at DNA-bound histones H3 and H4 by ChIP-chip along the ENCODE regions. In contrast to the global increases of histone acetylation, many genomic regions close to transcription start sites were deacetylated after butyrate exposure. In order to validate these findings, we found that both butyrate and trichostatin A treatment resulted in histone deacetylation at selected regions, while nucleosome loss or changes in histone H3 lysine 4 trimethylation (H3K4me3) did not occur in such locations. Furthermore, similar histone deacetylation events were observed when colon adenocarcinoma HT-29 cells were treated with butyrate. In addition, genes with deacetylated promoters were down-regulated by butyrate, and this was mediated at the transcriptional level by affecting RNA polymerase II (POLR2A) initiation/elongation. Finally, the global increase in acetylated histones was preferentially localized to the nuclear periphery, indicating that it might not be associated to euchromatin. Our results are significant for the evaluation of HDACi as anti-tumourogenic drugs, suggesting that previous models of action might need to be revised, and provides an explanation for the frequently observed repression of many genes during HDACi treatment.

Indexed as

AcetylationAdenocarcinomaButyratesCell Line, TumorColonic NeoplasmsEnzyme InhibitorsGene Expression ProfilingGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansNeoplasm ProteinsOligonucleotide Array Sequence AnalysisProtein Processing, Post-TranslationalButyratesEnzyme InhibitorsHistone Deacetylase InhibitorsHistone DeacetylasesHistonesNeoplasm Proteins

Identifiers

PMID17567991
PMCPMC1891332
OpenAlexW1971557910

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.