Evidence map›Paper›PMID 35872983›Full record

ArticleFrontiers in endocrinology2022

ERα and ERβ Homodimers in the Same Cellular Context Regulate Distinct Transcriptomes and Functions.

Dandan Song, Huan He, Rajitha Indukuri, Zhiqiang Huang, Lina Stepanauskaite, Indranil Sinha, Lars-Arne Haldosén, Chunyan Zhao, Cecilia Williams

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

  1. Estrogen Receptor Beta Isoforms Interplay Integrates Nuclear and Extra-Nuclear Signaling to Modulate Human Granulosa Cell Growth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  14. 17β-estradiol in colorectal cancer: friend or foe?Cell communication and signaling : CCS · 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

9 authors at 3 institutions in 2 countries.

Dandan SongClinical Medical Research Center for Women and Children Diseases, Maternal and Child Health Care Hospital of Shandong Province, Jinan, China.
Huan HeDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Rajitha IndukuriDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Zhiqiang HuangDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Lina StepanauskaiteDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Indranil SinhaDepartment of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Lars-Arne HaldosénDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Chunyan ZhaoDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Cecilia WilliamsDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Karolinska Institutet · SEJilin University · CNScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The two estrogen receptors ERα and ERβ are nuclear receptors that bind estrogen (E2) and function as ligand-inducible transcription factors. They are homologues and can form dimers with each other and bind to the same estrogen-response element motifs in the DNA. ERα drives breast cancer growth whereas ERβ has been reported to be anti-proliferative. However, they are rarely expressed in the same cells, and it is not fully investigated to which extent their functions are different because of inherent differences or because of different cellular context. To dissect their similarities and differences, we here generated a novel estrogen-dependent cell model where ERα homodimers can be directly compared to ERβ homodimers within the identical cellular context. By using CRISPR-cas9 to delete ERα in breast cancer MCF7 cells with Tet-Off-inducible ERβ expression, we generated MCF7 cells that express ERβ but not ERα. MCF7 (ERβ only) cells exhibited regulation of estrogen-responsive targets in a ligand-dependent manner. We demonstrated that either ER was required for MCF7 proliferation, but while E2 increased proliferation

Indexed as

Breast NeoplasmsEstrogen Receptor alphaEstrogen Receptor betaApoptosisCell Line, TumorEstradiolEstrogensFemaleG2 Phase Cell Cycle CheckpointsHumansLigandsOligonucleotide Array Sequence AnalysisTranscriptomeESR1 protein, humanESR2 protein, humanEstradiolEstrogen Receptor alphaEstrogen Receptor betaEstrogensLigandscistromeestradiol (17ß-estradiol)estrogen receptor alpha (ERα)estrogen receptor beta (ERß)proliferationRNA-Seq - RNA sequencing

Identifiers

PMID35872983
PMCPMC9299245
OpenAlexW4286615845

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.