Evidence map›Paper›PMID 34919781›Full record

ArticleMolecular oncology2022

Androgen receptor-mediated transcriptional repression targets cell plasticity in prostate cancer.

Éva Erdmann, Pauline Ould Madi Berthélémy, Félicie Cottard, Charlotte Zoe Angel, Edwige Schreyer, Tao Ye, Bastien Morlet, Luc Negroni, Bruno Kieffer, Jocelyn Céraline

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2022. 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
0.7field-weighted citation impact, top 27% 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, 11 citations in OpenAlex.

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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 3 institutions in 3 countries.

Éva ErdmannCNRS UMR 7104, INSERM U1258, IGBMC, University de Strasbourg, Illkirch, France.
Pauline Ould Madi BerthélémyCNRS UMR 7104, INSERM U1258, IGBMC, University de Strasbourg, Illkirch, France.
Félicie CottardUniversity of Freiburg, Freiburg im Breisgau, Germany.
Charlotte Zoe AngelGenomic Medicine Research Group, BMSRI, Ulster University, Belfast, UK.
Edwige SchreyerCNRS UMR 7104, INSERM U1258, IGBMC, University de Strasbourg, Illkirch, France.
Tao YeCNRS UMR 7104, INSERM U1258, IGBMC, University de Strasbourg, Illkirch, France.
Bastien MorletCNRS UMR 7104, INSERM U1258, IGBMC, University de Strasbourg, Illkirch, France.
Luc NegroniCNRS UMR 7104, INSERM U1258, IGBMC, University de Strasbourg, Illkirch, France.
Bruno KiefferCNRS UMR 7104, INSERM U1258, IGBMC, University de Strasbourg, Illkirch, France.
Jocelyn CéralineCNRS UMR 7104, INSERM U1258, IGBMC, University de Strasbourg, Illkirch, France.ORCID 0000-0001-6476-8797
Centre National de la Recherche Scientifique · FRUniversity of Freiburg · DEUniversity of Ulster · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Androgen receptor (AR) signaling remains the key therapeutic target in the management of hormone-naïve-advanced prostate cancer (PCa) and castration-resistant PCa (CRPC). Recently, landmark molecular features have been reported for CRPC, including the expression of constitutively active AR variants that lack the ligand-binding domain. Besides their role in CRPC, AR variants lead to the expression of genes involved in tumor progression. However, little is known about the specificity of their mode of action compared with that of wild-type AR (AR-WT). We performed AR transcriptome analyses in an androgen-dependent PCa cell line as well as cross-analyses with publicly available RNA-seq datasets and established that transcriptional repression capacity that was marked for AR-WT was pathologically lost by AR variants. Functional enrichment analyses allowed us to associate AR-WT repressive function to a panel of genes involved in cell adhesion and epithelial-to-mesenchymal transition. So, we postulate that a less documented AR-WT normal function in prostate epithelial cells could be the repression of a panel of genes linked to cell plasticity and that this repressive function could be pathologically abrogated by AR variants in PCa.

Indexed as

Prostatic Neoplasms, Castration-ResistantReceptors, AndrogenAndrogensCell Line, TumorCell PlasticityGene Expression Regulation, NeoplasticHumansMaleProstateAndrogensReceptors, Androgenandrogen receptorAR-V7cell plasticityEMTprostate cancertranscriptional repression

Identifiers

PMID34919781
PMCPMC9462842
OpenAlexW4200089510

What OpenQuestion holds

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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.