Evidence map›Paper›PMID 22184117›Full record

ArticleThe Journal of biological chemistry2012

The receptor tyrosine kinase EphA2 is a direct target gene of hypermethylated in cancer 1 (HIC1).

Bénédicte Foveau, Gaylor Boulay, Sébastien Pinte, Capucine Van Rechem, Brian R Rood, 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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Observational
  4. Article
  5. Article
  6. Downregulation of hypermethylated in cancer-1 byCancer cell international · 2018
    Article
  7. Article
  8. Article
  9. HIC1 modulates uveal melanoma progression by activating lncRNA-numb.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Eph receptors and ephrins as targets for cancer therapy.Journal of cellular and molecular medicine · 2012
    Review
  19. 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
  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 5 institutions in 2 countries.

Bénédicte FoveauCNRS UMR 8161, CNRS-Institut Pasteur de Lille-Université de Lille 1, 59021 Lille Cedex, France.
Gaylor Boulay
Sébastien Pinte
Capucine Van Rechem
Brian R Rood
Dominique Leprince
Université de Lille · FRCentre National de la Recherche Scientifique · FRGeorge Washington University · USInstitut de Biologie de Lille · FRInstitut Pasteur 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

The tumor suppressor gene hypermethylated in cancer 1 (HIC1), which encodes a transcriptional repressor, is epigenetically silenced in many human tumors. Here, we show that ectopic expression of HIC1 in the highly malignant MDA-MB-231 breast cancer cell line severely impairs cell proliferation, migration, and invasion in vitro. In parallel, infection of breast cancer cell lines with a retrovirus expressing HIC1 also induces decreased mRNA and protein expression of the tyrosine kinase receptor EphA2. Moreover, chromatin immunoprecipitation (ChIP) and sequential ChIP experiments demonstrate that endogenous HIC1 proteins are bound, together with the MTA1 corepressor, to the EphA2 promoter in WI38 cells. Taken together, our results identify EphA2 as a new direct target gene of HIC1. Finally, we observe that inactivation of endogenous HIC1 through RNA interference in normal breast epithelial cells results in the up-regulation of EphA2 and is correlated with increased cellular migration. To conclude, our results involve the tumor suppressor HIC1 in the transcriptional regulation of the tyrosine kinase receptor EphA2, whose ligand ephrin-A1 is also a HIC1 target gene. Thus, loss of the regulation of this Eph pathway through HIC1 epigenetic silencing could be an important mechanism in the pathogenesis of epithelial cancers.

Indexed as

Breast NeoplasmsCell Line, TumorDisease ProgressionDown-RegulationFibroblastsGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingHEK293 CellsHistone DeacetylasesHumansKruppel-Like Transcription FactorsMammary Glands, HumanPromoter Regions, GeneticProtein BindingReceptor, EphA2HIC1 protein, humanHistone DeacetylasesKruppel-Like Transcription FactorsMTA1 protein, humanReceptor, EphA2Repressor ProteinsRNA, MessengerTrans-Activators

Identifiers

PMID22184117
PMCPMC3285316
OpenAlexW2046674182

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.