Evidence map›Paper›PMID 24552459›Full record

ArticleBreast cancer research : BCR2014

Estrogen receptor beta as a novel target of androgen receptor action in breast cancer cell lines.

Pietro Rizza, Ines Barone, Domenico Zito, Francesca Giordano, Marilena Lanzino, Francesca De Amicis, Loredana Mauro, Diego Sisci, Stefania Catalano, Karin Dahlman Wright and 2 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

44 citing papers in PubMed, 111 citations in OpenAlex.

  1. Review
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  7. Modulating the Activity of Androgen Receptor for Treating Breast Cancer.International journal of molecular sciences · 2022
    Review
  8. Plants (Basel, Switzerland) · 2022
    Article
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  17. The expression and prognostic role of EBP1 and relationship with AR in HER2+ breast cancer.Virchows Archiv : an international journal of pathology · 2020
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  18. Review
  19. 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

12 authors at 3 institutions in 3 countries.

Pietro Rizza
Ines Barone
Domenico Zito
Francesca Giordano
Marilena Lanzino
Francesca De Amicis
Loredana Mauro
Diego Sisci
Stefania Catalano
Karin Dahlman Wright
Jan-Ake Gustafsson
Sebastiano Andò
University of Calabria · ITKarolinska Institutet · SEUniversity of Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe two isoforms of estrogen receptor (ER) alpha and beta play opposite roles in regulating proliferation and differentiation of breast cancers, with ER-alpha mediating mitogenic effects and ER-beta acting as a tumor suppressor. Emerging data have reported that androgen receptor (AR) activation inhibits ER-positive breast cancer progression mainly by antagonizing ER-alpha signaling. However, to date no studies have specifically evaluated a potential involvement of ER-beta in the inhibitory effects of androgens.

methodsER-beta expression was examined in human breast cancer cell lines using real-time PCR, Western blotting and small interfering RNA (siRNA) assays. Mutagenesis studies, electromobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) analysis were performed to assess the effects of mibolerone/AR on ER-beta promoter activity and binding.

resultsIn this study, we demonstrate that mibolerone, a synthetic androgen ligand, up-regulates ER-beta mRNA and protein levels in ER-positive breast cancer cells. Transient transfection experiments, using a vector containing the human ER-beta promoter region, show that mibolerone increases basal ER-beta promoter activity. Site-directed mutagenesis and deletion analysis reveal that an androgen response element (ARE), TGTTCT motif located at positions -383 and -377, is critical for mibolerone-induced ER-beta up-regulation in breast cancer cells. This occurs through an increased recruitment of AR to the ARE site within the ER-beta promoter region, along with an enhanced occupancy of RNA polymerase II. Finally, silencing of ER-beta gene expression by RNA interference is able to partially reverse the effects of mibolerone on cell proliferation, p21 and cyclin D1 expression.

conclusionsCollectively, these data provide evidence for a novel mechanism by which activated AR, through an up-regulation of ER-beta gene expression, inhibits breast cancer cell growth.

Indexed as

Breast NeoplasmsCell Line, TumorCell ProliferationCyclin D1Enzyme ActivationEstrogen Receptor alphaEstrogen Receptor betaFemaleHumansMCF-7 CellsMutagenesis, Site-DirectedNandrolonePromoter Regions, GeneticProtein BindingReceptors, Androgenrho GTP-Binding ProteinsCyclin D1ESR1 protein, humanEstrogen Receptor alphaEstrogen Receptor betamiboleroneNandroloneReceptors, Androgenrho GTP-Binding ProteinsRNA, MessengerRNA Polymerase IIRNA, Small InterferingTestosterone Congeners

Identifiers

PMID24552459
PMCPMC3978907
OpenAlexW2136833945

What OpenQuestion holds

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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.