Evidence map›Paper›PMID 24281001›Full record

ArticleBritish journal of cancer2014

p53-dependent and p53-independent anticancer effects of different histone deacetylase inhibitors.

J Sonnemann, C Marx, S Becker, S Wittig, C D Palani, O H Krämer, J F Beck

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. TH-302 (evofosfamide) monotherapy exerts anticancer activity in Ewing's sarcoma cells under hypoxia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Mechanisms of HDACs in cancer development.Frontiers in immunology · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021
    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

7 authors at 2 institutions in 1 country.

J SonnemannDepartment of Paediatric Haematology and Oncology, Jena University Hospital, Children's Clinic, Jena, Germany.
C MarxDepartment of Biochemistry, Center for Molecular Biomedicine, Institute for Biochemistry and Biophysics, Friedrich Schiller University of Jena, Jena, Germany.
S BeckerDepartment of Paediatric Haematology and Oncology, Jena University Hospital, Children's Clinic, Jena, Germany.
S WittigDepartment of Paediatric Haematology and Oncology, Jena University Hospital, Children's Clinic, Jena, Germany.
C D PalaniDepartment of Paediatric Haematology and Oncology, Jena University Hospital, Children's Clinic, Jena, Germany.
O H KrämerDepartment of Biochemistry, Center for Molecular Biomedicine, Institute for Biochemistry and Biophysics, Friedrich Schiller University of Jena, Jena, Germany.
J F BeckDepartment of Paediatric Haematology and Oncology, Jena University Hospital, Children's Clinic, Jena, Germany.
Jena University Hospital · DEFriedrich Schiller University Jena · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHistone deacetylase inhibitors (HDACi) are promising antineoplastic agents, but their precise mechanisms of actions are not well understood. In particular, the relevance of p53 for HDACi-induced effects has not been fully elucidated. We investigated the anticancer effects of four structurally distinct HDACi, vorinostat, entinostat, apicidin and valproic acid, using isogenic HCT-116 colon cancer cell lines differing in p53 status.

methodsEffects were assessed by MTT assay, flow-cytometric analyses of propidium iodide uptake, mitochondrial depolarisation and cell-cycle distribution, as well as by gene expression profiling.

resultsVorinostat was equally effective in p53 wild-type and null cells, whereas entinostat was less effective in p53 null cells. Histone deacetylase inhibitors treatment suppressed the expression of MDM2 and increased the abundance of p53. Combination treatments showed that vorinostat enhanced the cytotoxic activity of TRAIL and bortezomib, independent of the cellular p53 status. Investigations into the effects of an inhibitor of the sirtuin class of HDAC, tenovin-1, revealed that tenovin-1-mediated cell death hinged on p53.

conclusionThese results demonstrate that vorinostat activates p53, but does not require p53 for inducing its anticancer action. Yet they also demonstrate that entinostat-induced cytotoxic effects partially depend on p53, indicating that different HDACi have a different requirement for p53.

Indexed as

BenzamidesCell ProliferationColonic NeoplasmsFlow CytometryGene Expression Regulation, NeoplasticHCT116 CellsHistone Deacetylase InhibitorsHumansHydroxamic AcidsPeptides, CyclicProto-Oncogene Proteins c-mdm2PyridinesTumor Suppressor Protein p53Valproic AcidVorinostatapicidinBenzamidesentinostatHistone Deacetylase InhibitorsHydroxamic AcidsMDM2 protein, humanPeptides, CyclicProto-Oncogene Proteins c-mdm2PyridinesTP53 protein, humanTumor Suppressor Protein p53Valproic AcidVorinostat

Identifiers

PMID24281001
PMCPMC3915118
OpenAlexW1977068148

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.