Evidence map›Paper›PMID 16301995›Full record

ArticleOncogene2006

Identification of the p53 family-responsive element in the promoter region of the tumor suppressor gene hypermethylated in cancer 1.

C Britschgi, M Rizzi, T J Grob, M P Tschan, B Hügli, V A Reddy, A-C Andres, B E Torbett, A Tobler, M F Fey

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Identification of DMP1 as Novel p53 Repressed Transcriptional Target.International journal of molecular sciences · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Signification of Hypermethylated in Cancer 1 (HIC1) as Tumor Suppressor Gene in Tumor Progression.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012
    Article
  13. Article
  14. Article
  15. HIC1 regulates tumor cell responses to endocrine therapies.Molecular endocrinology (Baltimore, Md.) · 2009
    Article
  16. Article
  17. Article
  18. Article
  19. HIC1 (Hypermethylated in Cancer 1) epigenetic silencing in tumors.The international journal of biochemistry & cell biology · 2009
    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.

C BritschgiExperimental Oncology/Hematology, Inselspital and Department of Clinical Research, University of Bern, Bern, Switzerland.
M Rizzi
T J Grob
M P Tschan
B Hügli
V A Reddy
A-C Andres
B E Torbett
A Tobler
M F Fey

Funding

Blocking of HIV Chemokine Receptors By IntrabodiesR01AI049165 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI TORBETT, BRUCE EDWARD · 2001 to 2004
$1.5M
NIAID NIH HHS AI49165
6 · The paper itself

Abstract

The tumor suppressor gene hypermethylated in cancer 1 (HIC1), located on human chromosome 17p13.3, is frequently silenced in cancer by epigenetic mechanisms. Hypermethylated in cancer 1 belongs to the bric à brac/poxviruses and zinc-finger family of transcription factors and acts by repressing target gene expression. It has been shown that enforced p53 expression leads to increased HIC1 mRNA, and recent data suggest that p53 and Hic1 cooperate in tumorigenesis. In order to elucidate the regulation of HIC1 expression, we have analysed the HIC1 promoter region for p53-dependent induction of gene expression. Using progressively truncated luciferase reporter gene constructs, we have identified a p53-responsive element (PRE) 500 bp upstream of the TATA-box containing promoter P0 of HIC1, which is sequence specifically bound by p53 in vitro as assessed by electrophoretic mobility shift assays. We demonstrate that this HIC1 p53-responsive element (HIC1.PRE) is necessary and sufficient to mediate induction of transcription by p53. This result is supported by the observation that abolishing endogenous wild-type p53 function prevents HIC1 mRNA induction in response to UV-induced DNA damage. Other members of the p53 family, notably TAp73beta and DeltaNp63alpha, can also act through this HIC1.PRE to induce transcription of HIC1, and finally, hypermethylation of the HIC1 promoter attenuates inducibility by p53.

Indexed as

DNA MethylationPromoter Regions, GeneticAmino Acid SequenceBase SequenceCell Line, TumorDNA-Binding ProteinsDNA PrimersElectrophoretic Mobility Shift AssayGenes, p53Genes, ReporterHumansKruppel-Like Transcription FactorsMolecular Sequence DataReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSequence Homology, Nucleic AcidDNA-Binding ProteinsDNA PrimersHIC1 protein, humanKruppel-Like Transcription FactorsRNA, MessengerTranscription Factors

Identifiers

PMID16301995

What OpenQuestion holds

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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.