Evidence map›Paper›PMID 27323858›Full record

ArticleOncotarget2016

Tyrosine phosphorylation regulates ERβ ubiquitination, protein turnover, and inhibition of breast cancer.

Bin Yuan, Long Cheng, Kshama Gupta, Huai-Chin Chiang, Harshita B Gupta, Gangadhara R Sareddy, Degeng Wang, Kate Lathrop, Richard Elledge, Pei Wang and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Targeting Breast Cancer Stem Cells Using Naturally Occurring Phytoestrogens.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Estrogen receptor beta signaling in CD8Journal for immunotherapy of cancer · 2021
    Article
  9. Review
  10. 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

16 authors at 3 institutions in 2 countries.

Bin YuanDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing, China.
Long ChengDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing, China.
Kshama GuptaDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Huai-Chin ChiangDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Harshita B GuptaDepartment of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Gangadhara R SareddyDepartment of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Degeng WangDepartment of Epidemiology and Biostatistics, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Kate LathropDepartment of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Richard ElledgeDepartment of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Pei WangDepartment of Cellular and Structural Biology Cancer Therapy and Research Center, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Stanton McHardyCenter for Innovative Drug Discovery, University of Texas at San Antonio, San Antonio, TX, USA.
Ratna VadlamudiDepartment of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Tyler J CurielDepartment of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Yanfen HuDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Qinong YeDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing, China.
Rong LiDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
The University of Texas Health Science Center at San Antonio · USDalian Medical University · CNThe University of Texas at San Antonio · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Robin Jean Leach · 1991 to 2026
$59.1M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
Regulation of hormone production by matrix proteinsR01CA161349 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LI, RONG · 2012 to 2016
$1.5M
Genomic Basis of Biochemical Network TopologyR01LM010212 · NLM · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LI, RONG · 2010 to 2012
$806k
NCATS NIH HHS UL1 TR001120NCI NIH HHS P30 CA054174NCI NIH HHS R01 CA161349NLM NIH HHS R01 LM010212
6 · The paper itself

Abstract

Unlike estrogen receptor α (ERα) that predominantly promotes hormone-dependent breast tumor growth, ERβ exhibits antitumor effects in a variety of cancer types. We recently identified a phosphotyrosine residue in ERβ, but not ERα, that dictates ERβ transcriptional activity and antitumor function. We show here that this ER isotype-specific phosphotyrosine switch is important for regulating ERβ activity in cell proliferation, migration, and invasion. At the mechanistic level, phosphorylated ERβ, which recruits transcriptional coactivator p300, is in turn targeted by p300 for ubiquitination and proteasome-dependent protein turnover. Furthermore, ERβ-specific agonists such as S-equol enhance ERβ phosphorylation, suggesting a crosstalk between ligand- and posttranslational modification-dependent ERβ activation. Inhibition of xenograft tumor growth by S-equol is associated with reduced tumor Ki-67 expression and elevated ERβ tyrosine phosphorylation. Taken together, our data support the notion that phosphotyrosine-dependent ERβ signaling is an attractive target for anticancer treatment.

Indexed as

AnimalsAntineoplastic AgentsBreast NeoplasmsCell ProliferationCell SurvivalEstrogen Receptor betaFemaleHEK293 CellsHumansKi-67 AntigenLigandsMCF-7 CellsMiceMice, NudeNeoplasm Transplantationp300-CBP Transcription FactorsAntineoplastic AgentsESR2 protein, humanEstrogen Receptor betaKi-67 AntigenLigandsp300-CBP Transcription FactorsPhosphotyrosineProteasome Endopeptidase ComplexTyrosineantitumor activityERβprotein turnovertyrosine phosphorylationubiquitination

Identifiers

PMID27323858
PMCPMC5173158
OpenAlexW2437351717

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.