Evidence map›Paper›PMID 19117054›Full record

ArticleInternational journal of cancer2009

Estradiol downregulation of the tumor suppressor gene BTG2 requires estrogen receptor-alpha and the REA corepressor.

Sudipan Karmakar, Estrella A Foster, Carolyn L Smith

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Physiological genomics · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Female-specific hypertension loci on rat chromosome 13.Hypertension (Dallas, Tex. : 1979) · 2013
    Article
  10. Role of estrogen receptor α and β in preserving hippocampal function during aging.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  11. Article
  12. Estrogen receptor prevents p53-dependent apoptosis in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  13. 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

3 authors at 2 institutions in 1 country.

Sudipan KarmakarMolecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Estrella A Foster
Carolyn L Smith
Baylor College of Medicine · USBaylor University · US

Funding

ESTROGEN RECEPTOR-COREGULATOR FUNCTIONAL INTERACTIONSR01DK053002 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI SMITH, CAROLYN LOUISE · 1997 to 2018
$4.7M
Negative Regulation of Estrogen ReceptorsR01DK064038 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI SMITH, CAROLYN LOUISE · 2004 to 2007
$1.0M
NIDDK NIH HHS R01 DK053002NIDDK NIH HHS R01 DK064038
6 · The paper itself

Abstract

B-cell Translocation Gene 2 (BTG2/TIS21/PC3) is an anti-proliferative tumor suppressor gene whose expression is significantly reduced in breast carcinomas, and in MCF-7 and T-47D breast cancer cell lines treated with estradiol (E2). In this study the mechanisms involved in E2 down regulation of BTG2 gene expression were examined. Depletion of ERalpha by siRNA indicated that the receptor is required for E2 down regulation of BTG2 mRNA levels, and cycloheximide experiments indicated that the effect of E2 on BTG2 expression was independent of intermediary protein synthesis. Chromatin immunoprecipitation analyses revealed that ERalpha interacts with the BTG2 promoter in a ligand-independent fashion whereas transfection experiments indicated that ERalpha's DNA and ligand binding domains are required for E2 repression of BTG promoter activity. Surprisingly, histone deacetylase (HDACs) activity is essential for basal expression as evidenced by trichostatin A inhibition of BTG2 mRNA levels. Estradiol treatment did not alter histone H3 acetylation although it did induce displacement of RNA polymerase II from the BTG2 gene. Depletion of the ER specific corepressor REA (Repressor of Estrogen Receptor Activity) significantly abrogated E2-mediated BTG2 repression. Taken together, our results reveal a requirement of HDAC activity for basal BTG2 expression and the ERalpha-REA interaction for estrogen repression of the BTG2 gene. The ability of E2-bound ERalpha and REA to suppress BTG2 expression indicates a positive role for this corepressor in regulation of breast cancer cell proliferation.

Indexed as

Gene Expression Regulation, NeoplasticBase SequenceBreast NeoplasmsCell Line, TumorChromatin ImmunoprecipitationEstradiolEstrogen Receptor alphaGenes, Tumor SuppressorHistone DeacetylasesHumansImmediate-Early ProteinsLigandsMolecular Sequence DataProhibitinsProtein BindingProtein Structure, TertiaryBTG2 protein, humanEstradiolEstrogen Receptor alphaHistone DeacetylasesImmediate-Early ProteinsLigandsPHB2 protein, humanProhibitinsTumor Suppressor Proteins

Identifiers

PMID19117054
PMCPMC2669741
OpenAlexW2111985417

What OpenQuestion holds

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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.