Evidence map›Paper›PMID 30597111›Full record

ArticleNucleic acids research2019

The LIM protein Ajuba recruits DBC1 and CBP/p300 to acetylate ERα and enhances ERα target gene expression in breast cancer cells.

Beihui Xu, Qi Li, Ning Chen, Chunxiao Zhu, Qingrong Meng, Kasirajan Ayyanathan, Wenli Qian, Hao Jia, Jiamin Wang, Peihua Ni and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

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  16. LncRNA IFITM4P promotes immune escape by up-regulating PD-L1 via dual mechanism in oral carcinogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  17. Article
  18. ERα promotes transcription of tumor suppressor geneJournal of Zhejiang University. Science. B · 2021
    Article
  19. Article
  20. Article
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

11 authors at 4 institutions in 2 countries.

Beihui XuFaculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Qi LiHongqiao Institute of Medicine, Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Ning ChenFaculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Chunxiao ZhuDepartment of Allergy, Linyi Hospital of Traditional Chinese Medicine, Shandong Province, China.
Qingrong MengDepartment of Gynecology, Lanling People's Hospital, Shandong Province, China.
Kasirajan AyyanathanThe Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.
Wenli QianHongqiao Institute of Medicine, Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Hao JiaHongqiao Institute of Medicine, Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Jiamin WangHongqiao Institute of Medicine, Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Peihua NiFaculty of Medical Laboratory Science, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Zhaoyuan HouHongqiao Institute of Medicine, Tongren Hospital/Faculty of Basic Medicine, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Tongren Hospital · CNRuijin Hospital · CNLinyi City Chinese Medicine Hospital · CNThe Wistar Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogen/ERα signaling is critical for breast cancer progression and therapeutic treatments. Thus, identifying new regulators of this pathway will help to develop new therapeutics to overcome chemotherapy resistance of the breast cancer cells. Here, we report Ajuba directly interacts with ERα to potentiate ERα target gene expression, and biologically Ajuba promotes breast cancer cell growth and contributes to tamoxifen resistance of these cells. Ajuba constitutively binds the DBD and AF2 regions of ERα, and these interactions can be markedly enhanced by estrogen treatment. Mechanistically, Ajuba recruits DBC1 and CBP/p300 and forms a ternary complex to co-activate ERα transcriptional activity and concomitantly enhances ERα acetylation. Moreover, components of this complex can be found at endogenous promoters containing functional ERα responsive elements. Taken together, these data demonstrate that Ajuba functions as a novel co-activator of ERα and that Ajuba/DBC1/CBP/p300 ternary complex may be a new target for developing therapeutics to treat breast cancer.

Indexed as

Gene Expression Regulation, NeoplasticAcetylationBreast NeoplasmsCell Cycle ProteinsCell Line, TumorCell ProliferationEstrogen Receptor alphaEstrogensHumansLIM Domain ProteinsNerve Tissue Proteinsp300-CBP Transcription FactorsProtein BindingTamoxifenTranscription, GeneticTumor Suppressor ProteinsAJUBA protein, humanBRINP1 protein, humanCell Cycle ProteinsESR1 protein, humanEstrogen Receptor alphaEstrogensLIM Domain ProteinsNerve Tissue Proteinsp300-CBP Transcription FactorsTamoxifenTumor Suppressor Proteins

Identifiers

PMID30597111
PMCPMC6412004
OpenAlexW2907693827

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.