Evidence map›Paper›PMID 24441044›Full record

ArticleOncogene2015

SUPT6H controls estrogen receptor activity and cellular differentiation by multiple epigenomic mechanisms.

U Bedi, A H Scheel, M Hennion, Y Begus-Nahrmann, J Rüschoff, S A Johnsen

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 56 citations in OpenAlex.

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  12. International journal of molecular sciences · 2023
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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

6 authors at 2 institutions in 1 country.

U Bedi1] Center of Experimental Medicine, Department of Tumor Biology, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany [2] Institute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.
A H Scheel1] Institute of Pathology Nordhessen, Kassel, Germany [2] Center for Pathology and Forensic Medicine, Department of Pathology, University Medical Center Göttingen, Göttingen, Germany.
M HennionInstitute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.
Y Begus-NahrmannInstitute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.
J RüschoffInstitute of Pathology Nordhessen, Kassel, Germany.
S A Johnsen1] Center of Experimental Medicine, Department of Tumor Biology, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany [2] Institute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.
Universitätsmedizin Göttingen · DEUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The estrogen receptor alpha (ERα) is the central transcriptional regulator of ductal mammary epithelial lineage specification and is an important prognostic marker in human breast cancer. Although antiestrogen therapies are initially highly effective at treating ERα-positive tumors, a large number of tumors progress to a refractory, more poorly differentiated phenotype accompanied by reduced survival. A better understanding of the molecular mechanisms involved in the progression from estrogen-dependent to hormone-resistant breast cancer may uncover new targets for treatment and the discovery of new predictive markers. Recent studies have uncovered an important role for transcriptional elongation and chromatin modifications in controlling ERα activity and estrogen responsiveness. The human Suppressor of Ty Homologue-6 (SUPT6H) is a histone chaperone that links transcriptional elongation to changes in chromatin structure. We show that SUPT6H is required for estrogen-regulated transcription and the maintenance of chromatin structure in breast cancer cells, possibly in part through interaction with RNF40 and regulation of histone H2B monoubiquitination (H2Bub1). Moreover, we demonstrate that SUPT6H protein levels decrease with malignancy in breast cancer. Consistently, SUPT6H, similar to H2Bub1, is required for cellular differentiation and suppression of the repressive histone mark H3K27me3 on lineage-specific genes. Together, these data identify SUPT6H as a new epigenetic regulator of ERα activity and cellular differentiation.

Indexed as

Cell DifferentiationEpigenomicsBreast NeoplasmsCell Line, TumorChromatinEstrogen Receptor alphaFemaleHistonesHumansTranscription FactorsUbiquitinationChromatinESR1 protein, humanEstrogen Receptor alphaHistonesSUPT6H protein, humanTranscription Factors

Identifiers

PMID24441044
OpenAlexW2084913170

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.