Evidence map›Paper›PMID 18723112›Full record

ReviewThe international journal of biochemistry & cell biology2009

HIC1 (Hypermethylated in Cancer 1) epigenetic silencing in tumors.

Capucine Fleuriel, Majid Touka, Gaylor Boulay, Cateline Guérardel, Brian R Rood, Dominique Leprince

Open access · hybridAbstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

54 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. HIC1 suppresses Tumor Progression and Enhances CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Cellular taxonomy of Hic1Nature communications · 2022
    Article
  11. Article
  12. Histone Modification on Parathyroid Tumors: A Review of Epigenetics.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. δ-Catenin Participates in EGF/AKT/p21International journal of molecular sciences · 2021
    Article
  17. 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

6 authors at 4 institutions in 2 countries.

Capucine FleurielUniversité de Lille 1 et de Lille 2, Institut PASTEUR de LILLE, 59017 Lille Cedex, France.
Majid Touka
Gaylor Boulay
Cateline Guérardel
Brian R Rood
Dominique Leprince
Institut de Biologie de Lille · FRCentre National de la Recherche Scientifique · FRChildren's National · USUniversité de Lille · FR

Funding

Creation of a PDGF-C Autocrine Loop by HIC1 InactivationK08NS051477 · NINDS · CHILDREN'S NATIONAL MEDICAL CENTER · PI ROOD, BRIAN R · 2007 to 2011
$729k
NINDS NIH HHS 1K08NS051477NINDS NIH HHS K08 NS051477
6 · The paper itself

Abstract

HIC1 (Hypermethylated in Cancer 1), as it name implied, was originally isolated as a new candidate tumor suppressor gene located at 17p13.3 because it resides in a CpG island that is hypermethylated in many types of human cancers. HIC1 encodes a transcription factor associating an N-terminal BTB/POZ domain to five C-terminal Krüppel-like C(2)H(2) zinc finger motifs. In this review, we will begin by providing an overview of the current knowledge on HIC1 function, mainly gained from in vitro studies, as a sequence-specific transcriptional repressor interacting with a still growing range of HDAC-dependent and HDAC-independent corepressor complexes. We will then summarize the studies that have demonstrated frequent hypermethylation changes or losses of heterozygosity of the HIC1 locus in human cancers. Next, we will review animal models which have firmly established HIC1 as a bona fide tumor suppressor gene epigenetically silenced and functionally cooperating notably with p53 within a complex HIC1-p53-SIRT1 regulatory loop. Finally, we will discuss how this epigenetic inactivation of HIC1 might "addict" cancer cells to altered survival and signaling pathways or to lineage-specific transcription factors during the early stages of tumorigenesis.

Indexed as

Gene SilencingAnimalsHeterozygoteHistone DeacetylasesHumansKruppel-Like Transcription FactorsModels, BiologicalNeoplasmsSirtuinsTumor Suppressor Protein p53Zinc FingersHIC1 protein, humanHistone DeacetylasesKruppel-Like Transcription FactorsSirtuinsTumor Suppressor Protein p53

Identifiers

PMID18723112
PMCPMC2631403
OpenAlexW1977567422

What OpenQuestion holds

Textmetadata
LicenceTDM
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.