Evidence map›Paper›PMID 22315224›Full record

ArticleThe Journal of biological chemistry2012

Hypermethylated in cancer 1 (HIC1) recruits polycomb repressive complex 2 (PRC2) to a subset of its target genes through interaction with human polycomb-like (hPCL) proteins.

Gaylor Boulay, Marion Dubuissez, Capucine Van Rechem, Antoine Forget, Kristian Helin, Olivier Ayrault, Dominique Leprince

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  5. Article
  6. The Nuclear Lamina.Cold Spring Harbor perspectives in biology · 2022
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  7. Review
  8. Article
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  12. Article
  13. Article
  14. Regulation of Polycomb Repression byFrontiers in endocrinology · 2019
    Review
  15. Article
  16. Article
  17. Article
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  19. Article
  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 2 countries.

Gaylor BoulayCNRS UMR 8161, Institut de Biologie de Lille, Université Lille Nord de France, Institut Pasteur de Lille, Lille 59021, France.
Marion DubuissezCNRS UMR 8161, Institut de Biologie de Lille, Université Lille Nord de France, Institut Pasteur de Lille, Lille 59021, France.
Capucine Van RechemCNRS UMR 8161, Institut de Biologie de Lille, Université Lille Nord de France, Institut Pasteur de Lille, Lille 59021, France.
Antoine ForgetInstitut Curie, CNRS UMR 3306, INSERM U1005, Centre Universitaire, Orsay 91405, France, and.
Kristian HelinBRIC, University of Copenhagen, Ole Maaløes vej, 5, Dk-2200, Copenhagen, Denmark.
Olivier AyraultInstitut Curie, CNRS UMR 3306, INSERM U1005, Centre Universitaire, Orsay 91405, France, and.
Dominique LeprinceCNRS UMR 8161, Institut de Biologie de Lille, Université Lille Nord de France, Institut Pasteur de Lille, Lille 59021, France,. Electronic address: dominique.leprince@ibl.fr.
Centre National de la Recherche Scientifique · FRUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIC1 (hypermethylated in cancer 1) is a tumor suppressor gene epigenetically silenced or deleted in many human cancers. HIC1 is involved in regulatory loops modulating p53- and E2F1-dependent cell survival, growth control, and stress responses. HIC1 is also essential for normal development because Hic1-deficient mice die perinatally and exhibit gross developmental defects throughout the second half of development. HIC1 encodes a transcriptional repressor with five C(2)H(2) zinc fingers mediating sequence-specific DNA binding and two repression domains: an N-terminal BTB/POZ domain and a central region recruiting CtBP and NuRD complexes. By yeast two-hybrid screening, we identified the Polycomb-like protein hPCL3 as a novel co-repressor for HIC1. Using multiple biochemical strategies, we demonstrated that HIC1 interacts with hPCL3 and its paralog PHF1 to form a stable complex with the PRC2 members EZH2, EED, and Suz12. Confirming the implication of HIC1 in Polycomb recruitment, we showed that HIC1 shares some of its target genes with PRC2, including ATOH1. Depletion of HIC1 by siRNA interference leads to a partial displacement of EZH2 from the ATOH1 promoter. Furthermore, in vivo, ATOH1 repression by HIC1 is associated with Polycomb activity during mouse cerebellar development. Thus, our results identify HIC1 as the first transcription factor in mammals able to recruit PRC2 to some target promoters through its interaction with Polycomb-like proteins.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCarrier ProteinsCerebellumDNA-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinFemaleHistone-Lysine N-MethyltransferaseHumansKruppel-Like Transcription FactorsMiceNeoplasm ProteinsNuclear ProteinsPolycomb-Group ProteinsPolycomb Repressive Complex 2Repressor ProteinsATOH1 protein, humanAtoh1 protein, mouseBasic Helix-Loop-Helix ProteinsCarrier ProteinsDNA-Binding ProteinsEED protein, humanEed protein, mouseEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanEzh2 protein, mouseHIC1 protein, humanHic1 protein, mouseHistone-Lysine N-MethyltransferaseKruppel-Like Transcription FactorsNeoplasm ProteinsNuclear ProteinsPHF19 protein, humanPolycomb-Group ProteinsPolycomb Repressive Complex 2Repressor ProteinsSUZ12 protein, humanSuz12 protein, mouseTranscription Factors

Identifiers

PMID22315224
PMCPMC3323039
OpenAlexW2021130838

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.