Evidence map›Paper›PMID 20720010›Full record

ArticleThe Journal of biological chemistry2010

ATBF1 inhibits estrogen receptor (ER) function by selectively competing with AIB1 for binding to the ER in ER-positive breast cancer cells.

Xue-Yuan Dong, Xiaodong Sun, Peng Guo, Qunna Li, Masakiyo Sasahara, Yoko Ishii, Jin-Tang Dong

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

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  14. Shift work, DNA methylation and epigenetic age.International journal of epidemiology · 2019
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  18. Association study betweenJournal of exercise rehabilitation · 2017
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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

7 authors at 2 institutions in 2 countries.

Xue-Yuan DongFrom the Winship Cancer Institute and Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia 30322.
Xiaodong SunFrom the Winship Cancer Institute and Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia 30322.
Peng GuoFrom the Winship Cancer Institute and Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia 30322.
Qunna LiFrom the Winship Cancer Institute and Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia 30322.
Masakiyo SasaharaDepartment of Pathology, Graduate School of Medicine and Pharmaceutical Sciences for Research, University of Toyama, Toyama 930-0194, Japan.
Yoko IshiiDepartment of Pathology, Graduate School of Medicine and Pharmaceutical Sciences for Research, University of Toyama, Toyama 930-0194, Japan.
Jin-Tang DongFrom the Winship Cancer Institute and Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia 30322. Electronic address: j.dong@emory.edu.
Emory University · USUniversity of Toyama · JP

Funding

MOLECULAR DISSECTION OF 13Q14 IN PROSTATE CANCERR01CA085560 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI DONG, JIN-TANG · 2000 to 2010
$2.5M
NCI NIH HHS CA85560NCI NIH HHS R01 CA085560
6 · The paper itself

Abstract

Loss of the q22 band of chromosome 16 is a frequent genetic event in breast cancer, and the candidate tumor suppressor gene, ATBF1, has been implicated in breast cancer by genomic deletion, transcriptional down-regulation, and association with better prognostic parameters. In addition, estrogen receptor (ER)-positive breast cancer expresses a higher level of ATBF1, suggesting a role of ATBF1 in ER-positive breast cancer. In this study, we examined whether and how ATBF1 affects the ER function in breast cancer cells. We found that ATBF1 inhibited ER-mediated gene transcription, cell growth, and proliferation in ER-positive breast cancer cells. In vitro and in vivo immunoprecipitation experiments revealed that ATBF1 interacted physically with the ER and that multiple domains in both ATBF1 and ER proteins mediated the interaction. Furthermore, we demonstrated that ATBF1 inhibited ER function by selectively competing with the steroid receptor coactivator AIB1 but not GRIP1 or SRC1 for binding to the ER. These findings not only support the concept that ATBF1 plays a tumor-suppressive role in breast cancer, they also provide a mechanism for how ATBF1 functions as a tumor suppressor in breast cancer.

Indexed as

Breast NeoplasmsCarrier ProteinsCell Line, TumorFemaleGene DeletionHomeodomain ProteinsHumansMaleNerve Tissue ProteinsNuclear Receptor Coactivator 3Protein BindingReceptors, EstrogenTranscription, GeneticTumor Suppressor ProteinsCarrier ProteinsGRIP1 protein, humanHomeodomain ProteinsNCOA3 protein, humanNerve Tissue ProteinsNuclear Receptor Coactivator 3Receptors, EstrogenTumor Suppressor ProteinsZFHX3 protein, human

Identifiers

PMID20720010
PMCPMC2963406
OpenAlexW1978981428

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.