Evidence map›Paper›PMID 25096985›Full record

ArticleHormones & cancer2014

The G protein-coupled estrogen receptor-1, GPER-1, promotes fibrillogenesis via a Shc-dependent pathway resulting in anchorage-independent growth.

Hilary T Magruder, Jeffrey A Quinn, Jean E Schwartzbauer, Jonathan Reichner, Allan Huang, Edward J Filardo

Open access · bronzeAbstract read
In one paragraph

Article in Hormones & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  6. 17β-estradiol promotes extracellular vesicle release and selective miRNA loading in ERα-positive breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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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

6 authors at 3 institutions in 1 country.

Hilary T MagruderDivision of Hematology and Oncology, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI, 02903, USA.
Jeffrey A Quinn
Jean E Schwartzbauer
Jonathan Reichner
Allan Huang
Edward J Filardo
Brown University · USPrinceton University · USRhode Island Hospital · US

Funding

Molecular Analysis of Extracellular Matrix AssemblyR01CA160611 · NCI · PRINCETON UNIVERSITY · PI SCHWARZBAUER, JEAN E · 2012 to 2017
$1.6M
Study of GPR30: a novel estrogen receptor linked to breast cancer.R01CA119165 · NCI · RHODE ISLAND HOSPITAL · PI FILARDO, EDWARD J · 2007 to 2010
$1.2M
NCI NIH HHS CA119165-01A2NCI NIH HHS R01 CA119165NCI NIH HHS R01 CA160611
6 · The paper itself

Abstract

The G protein-coupled estrogen receptor-1, GPER-1, coordinates fibronectin (FN) matrix assembly and release of heparan-bound epidermal growth factor (HB-EGF). This mechanism of action results in the recruitment of FN-engaged integrin α5β1 to fibrillar adhesions and the formation of integrin α5β1-Shc adaptor protein complexes. Here, we show that GPER-1 stimulation of murine 4 T1 or human SKBR3 breast cancer cells with 17β-estradiol (E2β) promotes the formation of focal adhesions and actin stress fibers and results in increased cellular adhesion and haptotaxis on FN, but not collagen. These actions are also induced by the xenoestrogen, bisphenol A, and the estrogen receptor (ER) antagonist, ICI 182, 780, but not the inactive stereoisomer, 17α-estradiol (E2α). In addition, we show that GPER-1 stimulation of breast cancer cells allows for FN-dependent, anchorage-independent growth and FN fibril formation in "hanging drop" assays, indicating that these GPER-1-mediated actions occur independently of adhesion to solid substrata. Stable expression of Shc mutant Y317F lacking its primary tyrosyl phosphorylation site disrupts E2β-induced focal adhesion and actin stress fiber formation and abolishes E2β-enhanced haptotaxis on FN and anchorage-dependent growth. Collectively, these data demonstrate that E2β action via GPER-1 enhances cellular adhesivity and FN matrix assembly and allows for anchorage-independent growth, cellular events that may allow for cellular survival, and tumor progression.

Indexed as

ActinsAnimalsBenzhydryl CompoundsBisphenol A CompoundsBreast NeoplasmsCell AdhesionCell Growth ProcessesCell Line, TumorEpidermal Growth FactorEstradiolEstrogen Receptor ModulatorsFemaleFibronectinsFocal AdhesionsFulvestrantHumansActinsBenzhydryl Compoundsbisphenol ABisphenol A CompoundsEpidermal Growth FactorEstradiolEstrogen Receptor ModulatorsFibronectinsFulvestrantGPER1 protein, humanGPER1 protein, mousePhenolsReceptors, EstrogenReceptors, G-Protein-CoupledShc Signaling Adaptor Proteins

Identifiers

PMID25096985
PMCPMC4964789
OpenAlexW2070389588

What OpenQuestion holds

Textmetadata
LicenceTDM
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.