Evidence map›Paper›PMID 37442610›Full record

ArticleJournal of molecular cell biology2024

Estrogen receptor α-mediated signaling inhibits type I interferon response to promote breast carcinogenesis.

Li-Bo Cao, Zi-Lun Ruan, Yu-Lin Yang, Nian-Chao Zhang, Chuan Gao, Cheguo Cai, Jing Zhang, Ming-Ming Hu, Hong-Bing Shu

Open access · goldAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 14 citations in OpenAlex.

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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 1 institution in 1 country.

Li-Bo CaoDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Zi-Lun RuanDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.ORCID 0000-0003-0677-8377
Yu-Lin YangDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Nian-Chao ZhangDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Chuan GaoDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Cheguo CaiDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Jing ZhangDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.ORCID 0000-0001-6438-9113
Ming-Ming HuDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Hong-Bing ShuDepartment of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

Fundamental Research Funds for the Central Universities 2042022dx0003National Natural Science Foundation of China 32188101State Key R&D Program of China 2022YFA1304900
6 · The paper itself

Abstract

Estrogen receptor α (ERα) is an important driver and therapeutic target in ∼70% of breast cancers. How ERα drives breast carcinogenesis is not fully understood. In this study, we show that ERα is a negative regulator of type I interferon (IFN) response. Activation of ERα by its natural ligand estradiol inhibits IFN-β-induced transcription of downstream IFN-stimulated genes (ISGs), whereas ERα deficiency or the stimulation with its antagonist fulvestrant has opposite effects. Mechanistically, ERα induces the expression of the histone 2A variant H2A.Z to restrict the engagement of the IFN-stimulated gene factor 3 (ISGF3) complex to the promoters of ISGs and also interacts with STAT2 to disrupt the assembly of the ISGF3 complex. These two events mutually lead to the inhibition of ISG transcription induced by type I IFNs. In a xenograft mouse model, fulvestrant enhances the ability of IFN-β to suppress ERα+ breast tumor growth. Consistently, clinical data analysis reveals that ERα+ breast cancer patients with higher levels of ISGs exhibit higher long-term survival rates. Taken together, our findings suggest that ERα inhibits type I IFN response via two distinct mechanisms to promote breast carcinogenesis.

Indexed as

Breast NeoplasmsCarcinogenesisEstrogen Receptor alphaInterferon Type ISignal TransductionAnimalsCell Line, TumorEstradiolFemaleFulvestrantGene Expression Regulation, NeoplasticHistonesHumansInterferon-betaInterferon-Stimulated Gene Factor 3MiceESR1 protein, humanEstradiolEstrogen Receptor alphaFulvestrantHistonesInterferon-betaInterferon-Stimulated Gene Factor 3Interferon Type ISTAT2 Transcription Factorbreast cancerestrogen receptortype I interferon

Identifiers

PMID37442610
PMCPMC11066933
OpenAlexW4384129248

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.