Evidence map›Paper›PMID 14586398›Full record

ArticleOncogene2003

Tumor suppressor p53 inhibits transcriptional activation of invasion gene thromboxane synthase mediated by the proto-oncogenic factor ets-1.

Ella Kim, Willy Günther, Kimio Yoshizato, Hildegard Meissner, Srenja Zapf, Rolf M Nüsing, Hirotaka Yamamoto, Erwin G Van Meir, Wolfgang Deppert, Alf Giese

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Identification of DMP1 as Novel p53 Repressed Transcriptional Target.International journal of molecular sciences · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Mutant p53 and ETS2, a Tale of Reciprocity.Frontiers in oncology · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mutant p53: one name, many proteins.Genes & development · 2012
    Review
  18. Article
  19. Article
  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 5 institutions in 2 countries.

Ella KimDepartment of Neurosurgery, University Hospital Lübeck, Lübeck, Germany.
Willy Günther
Kimio Yoshizato
Hildegard Meissner
Srenja Zapf
Rolf M Nüsing
Hirotaka Yamamoto
Erwin G Van Meir
Wolfgang Deppert
Alf Giese
University Medical Center Hamburg-Eppendorf · DEUniversity of Lübeck · DEEmory University · USLeibniz Institute of Virology (LIV) · DEUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer formation and progression is a complex process determined by several mechanisms that promote cell growth, invasiveness, neo-angiogenesis, and render neoplastic cells resistant to apoptosis. The tumor suppressor p53 and the proto-oncogenic factor ets-1 are important regulators of such mechanisms. While it is well established that p53 and ets-1 influence various aspects of cell behavior by regulating the transcription of specific genes, little is known about the functional relationship between these transcription factors. We found that the gene encoding thromboxane synthase (TXSA), which we recently identified as a factor promoting invasion and resistance to apoptosis in gliomas, is a novel target gene for both p53 and ets-1. We demonstrate that p53 and ets-1 coregulate TXSA in an antagonistic and inter-related manner, with ets-1 being a potent transcriptional activator and p53 inhibiting ets-1-dependent transcription. Negative interference with ets-1 transcription requires functional p53 and is lost in mutant p53 proteins. We show that ets-1 and p53 associate physically in vitro and in vivo and that their interaction, rather than a direct binding of p53 to the TXSA promoter, is required for transcriptional repression of TXSA by wild-type p53. An important implication of our findings is that the loss of p53-mediated negative control over ets-1-dependent transcription may lead to the acquisition of an invasive phenotype in tumor cells.

Indexed as

Transcriptional ActivationBase SequenceCell Line, TumorDNAHumansMolecular Sequence DataPromoter Regions, GeneticProto-Oncogene Protein c-ets-1Proto-Oncogene ProteinsProto-Oncogene Proteins c-etsThromboxane-A SynthaseTranscription FactorsTumor Suppressor Protein p53DNAETS1 protein, humanProto-Oncogene Protein c-ets-1Proto-Oncogene ProteinsProto-Oncogene Proteins c-etsThromboxane-A SynthaseTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID14586398
OpenAlexW2153529101

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.