Evidence map›Paper›PMID 10962564›Full record

ArticleOncogene2000

Methylation of conserved CpG sites neighboring the beta retinoic acid response element may mediate retinoic acid receptor beta gene silencing in MCF-7 breast cancer cells.

A Arapshian, Y S Kuppumbatti, R Mira-y-Lopez

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. 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
2.0field-weighted citation impact, top 14% 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, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. EnhancedAdvanced pharmaceutical bulletin · 2016
    Article
  4. Exposures in early life: associations with DNA promoter methylation in breast tumors.Journal of developmental origins of health and disease · 2013
    Article
  5. Efficacy of the dietary histone deacetylase inhibitor butyrate alone or in combination with vitamin A against proliferation of MCF-7 human breast cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Overcoming retinoic acid-resistance of mammary carcinomas by diverting retinoic acid from PPARbeta/delta to RAR.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Methylation matters.Journal of medical genetics · 2001
    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

3 authors at 1 institution in 1 country.

A ArapshianDepartment of Medicine, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029-6574, USA.
Y S Kuppumbatti
R Mira-y-Lopez
Icahn School of Medicine at Mount Sinai · US

Funding

ABERRANT RETINOID SIGNALING IN BREAST CANCERR01CA054273 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI FARIAS, EDUARDO F · 1997 to 2010
$3.0M
NCI NIH HHS R01 CA54273
6 · The paper itself

Abstract

We investigated the mechanism of retinoic acid receptor (RAR) beta2 gene silencing in breast cancer cells. Transfection experiments indicated that MCF-7 cells transactivate an exogenous beta2 promoter (-1470/+156) to the same extent as MTSV1.7 breast epithelial cells, which express endogenous RARbeta2. This was true even in the context of replicated chromatin, suggesting a cis-acting rather than a trans-acting defect. Cytosine methylation, a cis-acting DNA modification, has been implicated in RARbeta2 silencing in cancer cells. Upon bisulfite genomic sequencing, we found that 3 CpG sites in the beta2 RARE region were variably methylated in MCF-7 cells but were not methylated in MTSV1.7 cells or in 2 MDA-MB-231 subclones that differed in RARbeta2 expression (high in clone A2, low in clone A4). However, the 5'-UTR region was hypermethylated in clone A4 relative to clone A2 cells. Following 5-azacytidine treatment, RA and trichostatin A markedly induced RARbeta2 expression in MCF-7 cells but not in MDA-MB-231 clone A4 cells. A beta2 RARE reporter construct in which the methylation-susceptible cytosines in the sense strand were replaced by thymine displayed marked loss of activity in a replicated chromatin-dependent manner. We conclude that cytosine methylation contributes to RARbeta2 gene silencing in MCF-7 cells and that methylation of the RARE region may be particularly important. Oncogene (2000) 19, 4066 - 4070.

Indexed as

CpG IslandsDNA MethylationGene Expression Regulation, NeoplasticAdenocarcinomaAzacitidineBase SequenceBreast NeoplasmsClone CellsFemaleGene SilencingGenes, ReporterHumansMolecular Sequence DataNeoplasm ProteinsPromoter Regions, GeneticReceptors, Retinoic AcidAzacitidineNeoplasm ProteinsReceptors, Retinoic Acidretinoic acid receptor betaTretinoin

Identifiers

PMID10962564
OpenAlexW2316388803

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.