Evidence map›Paper›PMID 16980581›Full record

ArticleGenes & development2006

A cell-type-specific transcriptional network required for estrogen regulation of cyclin D1 and cell cycle progression in breast cancer.

Jérôme Eeckhoute, Jason S Carroll, Timothy R Geistlinger, Maria I Torres-Arzayus, Myles Brown

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed
–field-weighted citation impact
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

173 citing papers in PubMed, 307 citations in OpenAlex.

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  14. The Role of CD4/6 Inhibitors in Breast Cancer Treatment.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Article
  17. Updated Review Article: Cyclin-Dependent Kinase 4/6 Inhibitor Impact, FDA Approval, and Resistance Pathways.The Journal of pharmacy technology : jPT : official publication of the Association of Pharmacy Technicians · 2023
    Review
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  19. Article
  20. Review

113 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

5 authors at 3 institutions in 1 country.

Jérôme EeckhouteDivision of Molecular and Cellular Oncology, Department of Medical Oncology, Dana-Farber Cancer Institute and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Jason S Carroll
Timothy R Geistlinger
Maria I Torres-Arzayus
Myles Brown
Dana-Farber Cancer Institute · USHarvard University · USBrigham and Women's Hospital · 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 ActionR56DK074967 · NIDDK · DANA-FARBER CANCER INST · PI BROWN, MYLES A · 2006 to 2006
$420k
NCI NIH HHS P01 CA080111NCI NIH HHS P01 CA80111NIDDK NIH HHS R56 DK074967
6 · The paper itself

Abstract

Estrogen stimulates the proliferation of the most common type of human breast cancer that expresses estrogen receptor alpha (ERalpha) through the activation of the cyclin D1 (CCND1) oncogene. However, our knowledge of ERalpha transcriptional mechanisms remains limited. Hence, it is still elusive why ERalpha ectopically expressed in ER-negative breast cancer cells (BCC) is functional on ectopic reporter constructs but lacks activity on many endogenous target genes, including CCND1. Here, we show that estradiol (E2) stimulation of CCND1 expression in BCC depends on a novel cell-type-specific enhancer downstream from the CCND1 coding region, which is the primary ERalpha recruitment site in estrogen-responsive cells. The pioneer factor FoxA1 is specifically required for the active chromatin state of this enhancer and as such is crucial for both CCND1 expression and subsequent cell cycle progression. Interestingly, even in BCC, CCND1 levels and proliferation are tightly controlled by E2 through the establishment of a negative feedforward loop involving the induction of NFIC, a putative tumor suppressor capable of directly repressing CCND1 transcription. Taken together, our results reveal an estrogen-regulated combinatorial network including cell-specific cis- and trans-regulators of CCND1 expression where ERalpha collaborates with other transcription factors associated with the ER-positive breast cancer phenotype, including FoxA1 and NFIC.

Indexed as

Adaptor Proteins, Signal TransducingBreast NeoplasmsCell CycleCell Line, TumorCyclin D1DNA Polymerase IIEnhancer Elements, GeneticEstradiolEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-alphaHumansLIM Domain ProteinsMicrofilament ProteinsModels, BiologicalAdaptor Proteins, Signal TransducingCyclin D1DNA Polymerase IIEstradiolEstrogen Receptor alphaFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaLIM Domain ProteinsMicrofilament ProteinsNFIC protein, humanNFI Transcription FactorsPDLIM5 protein, human

Identifiers

PMID16980581
PMCPMC1578675
OpenAlexW2129036353

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.