Evidence map›Paper›PMID 31504401›Full record

ArticleEndocrinology2019

Genomic Function of Estrogen Receptor β in Endometriosis.

Sang Jun Han, Jiyeun E Lee, Yeon Jean Cho, Mi Jin Park, Bert W O'Malley

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  19. N-Myc and STAT Interactor is an Endometriosis Suppressor.International journal of molecular sciences · 2024
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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 1 institution in 2 countries.

Sang Jun HanDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Jiyeun E LeeDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Yeon Jean ChoDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Mi Jin ParkDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Bert W O'MalleyDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Baylor College of Medicine · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
REPRODUCTIVE HORMONES: BIOLOGICAL AND MOLECULAR ACTIONSR01HD008188 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI DAVID M LONARD, JOHN P LYDON · 1985 to 2026
$16.3M
The ERbeta/SRC-1 isoform complex drives endometriosis progression R01HD082786 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI O'MALLEY, BERT W · 2014 to 2018
$1.1M
NCI NIH HHS P30 CA125123NICHD NIH HHS R01 HD008188NICHD NIH HHS R01 HD082786
6 · The paper itself

Abstract

Estrogen receptor (ER) β plays a critical role in endometriosis progression because cytoplasmic ERβ stimulates proinflammatory signaling in ectopic lesions and prevents apoptosis to promote their survival. However, the role of "nuclear ERβ" in endometriosis progression is not known. This critical knowledge gap obscures our understanding of the full molecular etiology of ERβ-mediated endometriosis progression. To fill this void, we generated an ERβ-regulated transcriptome and ERβ cistrome in ectopic lesions and the eutopic endometrium of mice with endometriosis by using a new endometrium-specific FLAG-tagged human ERβ overexpression mouse model. The integration of these omics data sets revealed that ERβ stimulated the proliferation activities of ectopic lesions and the eutopic endometrium by directly upregulating MYC and E2 transcription factor target genes and genes associated with the G2/M transition. Additionally, ERβ stimulated gene expression associated with TNFα/nuclear factor κB (NF-κB) signaling, epithelial-mesenchymal transition, reactive oxygen species signaling, IL-6/Janus kinase (JAK)/signal transducer and activator of transcription (STAT)3 signaling, and hypoxia signaling and suppressed IFNα signaling in ectopic lesions to enhance endometriosis progression. ERβ also stimulated gene expression associated with the unfolded protein response and IL-6/JAK/STAT3 inhibitory signaling and suppressed TNFα/NF-κB signaling in the eutopic endometrium to cause endometriosis-associated endometrial dysfunction. Therefore, nuclear ERβ-regulated gene networks provide critical clues to understand the molecular etiology and complexity of endometriosis and endometriosis-associated endometrial dysfunction.

Indexed as

Gene Expression RegulationGene Regulatory NetworksAnimalsEndometriosisEndometriumEstrogen Receptor betaFemaleHumansInterferonsMice, Inbred C57BLEstrogen Receptor betaInterferons

Identifiers

PMID31504401
PMCPMC6773435
OpenAlexW2972709345

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.