Evidence map›Paper›PMID 22136382›Full record

ArticleCancer cell international2011

Down-regulation of DcR2 sensitizes androgen-dependent prostate cancer LNCaP cells to TRAIL-induced apoptosis.

David Vindrieux, Marie Réveiller, Jacqueline Chantepie, Sadok Yakoub, Catherine Deschildre, Alain Ruffion, Marian Devonec, Mohamed Benahmed, Renée Grataroli

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2011. 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
0.8field-weighted citation impact, top 28% 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, 18 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

9 authors at 6 institutions in 3 countries.

David Vindrieux *UMR Inserm U1052/CNRS 5286, Centre Léon Bérard, 28 rue Laënnec, 69373 Lyon Cedex 08, France.
Marie Réveiller *NYU Langone Medical Center, Department of Medicine and Pathology, 423 East 23 rd street, New York, NY 10010, USA.
Jacqueline ChantepieInserm, retired.
Sadok YakoubUnité de nutrition humaine, UMR INRA U1019/Université Clermont 1, Centre de recherche INRA de Clermont-Ferrand/Theix, 63122 St Genès Champanelle, France.
Catherine DeschildreU851 Inserm-UCBL-HCL, Tour INSERM CERVI, 21 avenue Tony Garnier, 69365 Lyon, France.
Alain RuffionService d'Urologie, Centre Hospitalier Lyon Sud, 165 chemin du grand Revoyet, 69921 Oullins, France.
Marian DevonecService d'Urologie, Centre Hospitalier Lyon Sud, 165 chemin du grand Revoyet, 69921 Oullins, France.
Mohamed BenahmedU895 Inserm, Université de Nice-Sophia Antipolis, UFR Medecine, 151 route Saint Antoine de Ginestiere, 06204 Nice, France.
Renée GrataroliSF Biosciences Gerland-Lyon Sud, CNRS UMS3444/Inserm US8, Université Claude Bernard Lyon 1, 50 avenue Tony Garnier, 69366 Lyon, France.
Hôpital Lyon Sud · FRInserm · FRUniversité Claude Bernard Lyon 1 · FRCentre National de la Recherche Scientifique · FRInstitut National de la Recherche Agronomique · MANYU Langone Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDysregulation of many apoptotic related genes and androgens are critical in the development, progression, and treatment of prostate cancer. The differential sensitivity of tumour cells to TRAIL-induced apoptosis can be mediated by the modulation of surface TRAIL receptor expression related to androgen concentration. Our previous results led to the hypothesis that downregulation of TRAIL-decoy receptor DcR2 expression following androgen deprivation would leave hormone sensitive normal prostate cells vulnerable to the cell death signal generated by TRAIL via its pro-apoptotic receptors. We tested this hypothesis under pathological conditions by exploring the regulation of TRAIL-induced apoptosis related to their death and decoy receptor expression, as also to hormonal concentrations in androgen-sensitive human prostate cancer, LNCaP, cells.

resultsIn contrast to androgen-insensitive PC3 cells, decoy (DcR2) and death (DR5) receptor protein expression was correlated with hormone concentrations and TRAIL-induced apoptosis in LNCaP cells. Silencing of androgen-sensitive DcR2 protein expression by siRNA led to a significant increase in TRAIL-mediated apoptosis related to androgen concentration in LNCaP cells.

conclusionsThe data support the hypothesis that hormone modulation of DcR2 expression regulates TRAIL-induced apoptosis in LNCaP cells, giving insight into cell death induction in apoptosis-resistant hormone-sensitive tumour cells from prostate cancer. TRAIL action and DcR2 expression modulation are potentially of clinical value in advanced tumour treatment.

Identifiers

PMID22136382
PMCPMC3286382
OpenAlexW2111164135

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Registered trials

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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.