Evidence map›Paper›PMID 19015639›Full record

ArticleOncogene2009

Requirement for chromatin-remodeling complex in novel tumor suppressor HIC1-mediated transcriptional repression and growth control.

B Zhang, K J Chambers, D Leprince, D V Faller, S Wang

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Neuromolecular responses to social challenge: common mechanisms across mouse, stickleback fish, and honey bee.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  4. Article
  5. Article
  6. 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
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. HIC1 regulates tumor cell responses to endocrine therapies.Molecular endocrinology (Baltimore, Md.) · 2009
    Article
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

B ZhangCancer Research Center, Boston University School of Medicine, Boston, MA 02118, USA.
K J Chambers
D Leprince
D V Faller
S Wang
Boston University · USCancer Research Center · USCentre National de la Recherche Scientifique · FR

Funding

Signal Transduction by Androgen in Prostate CellsR01CA101992 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FALLER, DOUGLAS V · 2004 to 2013
$2.4M
Role of Prohibitin in Mediating Suppression of Breast Cancer Growth by Estrogen *R03CA102940 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WANG, SHENG · 2003 to 2004
$162k
NCI NIH HHS CA101992NCI NIH HHS CA102940NCI NIH HHS R01 CA101992NCI NIH HHS R03 CA102940
6 · The paper itself

Abstract

HIC1 is a newly discovered tumor suppressor and transcriptional repressor that is frequently silenced in human tumors. HIC1 protein expression has been linked to better outcomes in breast cancers. The molecular mechanism underlying HIC1-mediated transcriptional and growth suppression, and the relevant targets of HIC1-mediated transcriptional modulation, is currently unclear. We have identified an HIC1 DNA-binding site in E2F-responsive gene promoters and demonstrate that HIC1 targets E2F-responsive genes for transcriptional regulation and growth suppression. We and others have recently discovered that Brg1, a central component of the SWI/SNF chromatin-remodeling family, is required for the transcriptional regulation of multiple cell cycle control-related genes, including E2F-responsive promoters. We studied HIC1 interactions with, and dependence upon, Brg1 activity, and found that HIC1 can recruit Brg1 to E2F-responsive promoters and that its transcriptional repression of these genes is dependent upon Brg1. These data indicate that HIC1 is a central molecule in a novel mechanism controlling cell growth and that the disruption of this HIC1-mediated pathway may lead to abnormal cell proliferation and, ultimately, cancer.

Indexed as

Cell ProliferationChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneDNA HelicasesDown-RegulationE2F1 Transcription FactorGenes, Tumor SuppressorHumansKruppel-Like Transcription FactorsNeoplasmsNuclear ProteinsProtein BindingTranscription FactorsTranscription, GeneticTumor Cells, CulturedChromosomal Proteins, Non-HistoneDNA HelicasesE2F1 protein, humanE2F1 Transcription FactorHIC1 protein, humanKruppel-Like Transcription FactorsNuclear ProteinsSMARCA4 protein, humanSWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID19015639
PMCPMC2636853
OpenAlexW2063462611

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.