Evidence map›Paper›PMID 18818283›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2008

Unique ERalpha cistromes control cell type-specific gene regulation.

Susan A Krum, Gustavo A Miranda-Carboni, Mathieu Lupien, Jerome Eeckhoute, Jason S Carroll, Myles Brown

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

82 citing papers in PubMed, 126 citations in OpenAlex.

  1. Review
  2. Article
  3. Regulation and Function of FOXC1 in Osteoblasts.Journal of developmental biology · 2023
    Article
  4. The SET oncoprotein promotes estrogen-induced transcription by facilitating establishment of active chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Profile of Myles Brown.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. GATA4 Directly RegulatesJBMR plus · 2018
    Article
  17. Article
  18. Embryonic transcription factor SOX9 drives breast cancer endocrine resistance.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. Maturing of the nuclear receptor family.The Journal of clinical investigation · 2017
    Review
  20. Review

22 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Susan A KrumDivision of Molecular and Cellular Oncology, Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, D730, Boston, Massachusetts 02115, USA.
Gustavo A Miranda-Carboni
Mathieu Lupien
Jerome Eeckhoute
Jason S Carroll
Myles Brown
Dana-Farber Cancer Institute · USCancer Research UK · GBUniversity of California, Los Angeles · US

Funding

Use of Organotypic and Mammary Gland Models to Investigate the Outcomes of ClonalP01CA080111 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DILLON, DEBORAH · 1999 to 2018
$36.0M
Comprehensive Analysis of Estrogen Receptor Genomic ActionR01DK074967 · NIDDK · DANA-FARBER CANCER INST · PI BROWN, MYLES A · 2007 to 2011
$2.9M
NCI NIH HHS P01 CA8011105NIDDK NIH HHS R01 DK074967NIDDK NIH HHS R01DK074967
6 · The paper itself

Abstract

Estrogens play an important role in normal physiology and in a variety of pathological states involving diverse tissues including breast and bone. The mechanism by which estrogens exert cell type- and disease-specific effects, however, remains to be explained. We have compared the gene expression profile of the MCF7 breast cancer cell line with that of the osteoblast-like cell line U2OS-ERalpha by expression microarrays. We find that fewer than 10% of the 17beta-estradiol (E2)-regulated genes are common to both cell types. We have validated this in primary calvarial osteoblasts. To dissect the mechanism underlying the cell type-specific E2 regulation of gene expression in MCF7 and U2OS-ERalpha cells, we compared the ERalpha binding sites on DNA in the two cell types by performing chromatin immunoprecipitation (ChIP) on genomic tiling arrays (ChIP-on-chip). Consistent with the distinct patterns of E2-regulated gene expression in these two cell lines, we find that the vast majority of ERalpha binding sites are also cell type specific and correlate both in position and number with cell type-specific gene regulation. Interestingly, although the forkhead factor FoxA1 plays a critical role in defining the ERalpha cistrome in MCF7 cells, it is not expressed in U2OS-ERalpha cells, and forkhead motifs are not enriched in the ERalpha cistrome in these cells. Finally, the ERalpha cistromes are correlated with cell type-specific epigenetic histone modifications. These results support a model for the cell type-specific action of E2 being driven primarily through specific ERalpha occupancy of epigenetically marked cis-regulatory regions of target genes.

Indexed as

Alkaline PhosphataseBinding SitesBreast NeoplasmsCell LineCell Line, TumorChromatinChromatin ImmunoprecipitationDNADNA, NeoplasmEpigenesis, GeneticEstradiolEstrogen Receptor alphaFemaleGene Expression ProfilingGenetic Complementation TestHepatocyte Nuclear Factor 3-alphaAlkaline PhosphataseChromatinDNADNA, NeoplasmEstradiolEstrogen Receptor alphaFOXA1 protein, humanHepatocyte Nuclear Factor 3-alpha

Identifiers

PMID18818283
PMCPMC2582540
OpenAlexW1993888034

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.