Evidence map›Paper›PMID 26646587›Full record

ArticleOncotarget2016

GPER is involved in the stimulatory effects of aldosterone in breast cancer cells and breast tumor-derived endothelial cells.

Damiano Cosimo Rigiracciolo, Andrea Scarpelli, Rosamaria Lappano, Assunta Pisano, Maria Francesca Santolla, Silvia Avino, Paola De Marco, Benedetta Bussolati, Marcello Maggiolini, Ernestina Marianna De Francesco

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 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 69 citations in OpenAlex.

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  18. G protein-coupled estrogen receptor 1 as a novel regulator of blood pressure.American journal of physiology. Renal physiology · 2020
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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

10 authors at 2 institutions in 1 country.

Damiano Cosimo RigiraccioloDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Andrea ScarpelliDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Rosamaria LappanoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Assunta PisanoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Maria Francesca SantollaDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Silvia AvinoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Paola De MarcoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Benedetta BussolatiDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Turin, Italy.
Marcello MaggioliniDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Ernestina Marianna De FrancescoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
University of Calabria · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aldosterone induces relevant effects binding to the mineralcorticoid receptor (MR), which acts as a ligand-gated transcription factor. Alternate mechanisms can mediate the action of aldosterone such as the activation of epidermal growth factor receptor (EGFR), MAPK/ERK, transcription factors and ion channels. The G-protein estrogen receptor (GPER) has been involved in the stimulatory effects of estrogenic signalling in breast cancer. GPER has been also shown to contribute to certain responses to aldosterone, however the role played by GPER and the molecular mechanisms implicated remain to be fully understood. Here, we evaluated the involvement of GPER in the stimulatory action exerted by aldosterone in breast cancer cells and breast tumor derived endothelial cells (B-TEC). Competition assays, gene expression and silencing studies, immunoblotting and immunofluorescence experiments, cell proliferation and migration were performed in order to provide novel insights into the role of GPER in the aldosterone-activated signalling. Our results demonstrate that aldosterone triggers the EGFR/ERK transduction pathway in a MR- and GPER-dependent manner. Aldosterone does not bind to GPER, it however induces the direct interaction between MR and GPER as well as between GPER and EGFR. Next, we ascertain that the up-regulation of the Na+/H+ exchanger-1 (NHE-1) induced by aldosterone involves MR and GPER. Biologically, both MR and GPER contribute to the proliferation and migration of breast and endothelial cancer cells mediated by NHE-1 upon aldosterone exposure. Our data further extend the current knowledge on the molecular mechanisms through which GPER may contribute to the stimulatory action elicited by aldosterone in breast cancer.

Indexed as

AldosteroneBreast NeoplasmsCation Transport ProteinsCell Line, TumorCell MovementCell ProliferationEndothelial CellsErbB ReceptorsGene ExpressionHumansImmunoblottingMicroscopy, FluorescenceProtein BindingReceptors, EstrogenReceptors, G-Protein-CoupledReceptors, MineralocorticoidAldosteroneCation Transport ProteinsErbB ReceptorsGPER1 protein, humanReceptors, EstrogenReceptors, G-Protein-CoupledReceptors, MineralocorticoidSLC9A1 protein, humanSodium-Hydrogen Exchanger 1Sodium-Hydrogen Exchangersaldosteronebreast cancer cellsbreast tumor-derived endothelial cellsGPERmineralcorticoid receptorPathology Section

Identifiers

PMID26646587
PMCPMC4807985
OpenAlexW2188222728

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.