Evidence map›Paper›PMID 15077164›Full record

ArticleOncogene2004

HDAC inhibitors trigger apoptosis in HPV-positive cells by inducing the E2F-p73 pathway.

Patrick Finzer, Andreas Krueger, Michael Stöhr, Dirk Brenner, Ubaldo Soto, Christian Kuntzen, Peter H Krammer, Frank Rösl

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

20 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. Do or Die: HPV E5, E6 and E7 in Cell Death Evasion.Pathogens (Basel, Switzerland) · 2022
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. International journal of molecular sciences · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Histone deacetylases in viral infections.Clinical epigenetics · 2010
    Article
  17. Article
  18. Combination of proteasome and HDAC inhibitors for uterine cervical cancer treatment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  19. Review
  20. Apoptotic and autophagic cell death induced by histone deacetylase inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2004
    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

8 authors at 2 institutions in 2 countries.

Patrick FinzerDeutsches Krebsforschungszentrum, Forschungsschwerpunkt Angewandte Tumorvirologie, Abteilung Virale Transformationsmechanismen, Im Neuenheimer Feld 242, 69120 Heidelberg, Germany. p.finzer@dkfz.de
Andreas Krueger
Michael Stöhr
Dirk Brenner
Ubaldo Soto
Christian Kuntzen
Peter H Krammer
Frank Rösl
DKFZ-ZMBH Alliance · DEDana-Farber Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase (HDAC) inhibitors induce an intrinsic type of apoptosis in human papillomavirus (HPV)-positive cells by disrupting the mitochondrial transmembrane potential (deltapsim). Loss of deltapsim was only detected in E7, but not in E6 oncogene-expressing cells. HDAC inhibition led to a time-dependent degradation of the pocket proteins pRb, p107 and p130, releasing 'free' E2F-1 following initial G1 arrest. Inhibition of proteasomal proteolysis, but not of caspase activity rescued pRb from degradation and functionally restored its inhibitory effect on the cyclin E gene, known to be suppressed by pRb-E2F-1 in conjunction with HDAC1. Using siRNA targeted against p53, E2F-1 still triggered apoptosis by inducing the E2F-responsive proapoptotic alpha- and beta-isoforms of p73. These data may determine future therapeutic strategies in which HDAC inhibitors can effectively eliminate HPV-positive cells by an apoptotic route that does not rely on the reactivation of the 'classical' p53 pathway through a preceding shut-off of viral gene expression.

Indexed as

Cell Cycle ProteinsHistone Deacetylase InhibitorsApoptosisBase SequenceDNA-Binding ProteinsDNA PrimersE2F1 Transcription FactorE2F Transcription FactorsEnzyme InhibitorsGenes, Tumor SuppressorHeLa CellsHumansIntracellular MembranesMembrane PotentialsMitochondriaNuclear ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA PrimersE2F1 protein, humanE2F1 Transcription FactorE2F Transcription FactorsEnzyme InhibitorsHistone Deacetylase InhibitorsNuclear ProteinsProtein IsoformsReceptors, FcRNA, Small InterferingTP73 protein, humanTranscription FactorsTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID15077164
OpenAlexW2067750642

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.