Evidence map›Paper›PMID 24243687›Full record

ArticleEndocrine-related cancer2014

TBLR1 as an androgen receptor (AR) coactivator selectively activates AR target genes to inhibit prostate cancer growth.

Garrett Daniels, Yirong Li, Lan Lin Gellert, Albert Zhou, Jonathan Melamed, Xinyu Wu, Xinming Zhang, David Zhang, Daniel Meruelo, Susan K Logan and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Endocrine-related cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 37 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

12 authors at 3 institutions in 3 countries.

Garrett DanielsDepartment of Pathology, New York University School of Medicine, New York, New York, USA Department of Pathology, Mount Sinai School of Medicine, New York, New York, USA NYU Cancer Institute, Department of Urology, Department of Pharmacology, New York Harbor Healthcare System, New York University School of Medicine, New York, New York, USA.
Yirong Li
Lan Lin Gellert
Albert Zhou
Jonathan Melamed
Xinyu Wu
Xinming Zhang
David Zhang
Daniel Meruelo
Susan K Logan
Ross Basch
Peng Lee
University of York · GBCancer Institute (WIA) · INVA NY Harbor Healthcare System · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
INSTITUTIONAL CLINICAL AND TRANSLATIONAL SCIENCE AWARDUL1RR029893 · NCRR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CRONSTEIN, BRUCE NEIL · 2009 to 2011
$17.7M
TRAINING PROGRAM IN MOLECULAR ONCOLOGY &IMMUNOLOGYT32CA009161 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CARROLL, WILLIAM L., LEVY, DAVID E · 1985 to 2020
$13.3M
Signaling Pathway Alterations in the Racial Disparity of Prostate CancerU01CA149556 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LEE, PENG, ZHANG, DAVID Y · 2011 to 2016
$1.9M
A signal pathway-based signature for metastatic prostate cancerI01BX001505 · VA · VA MEDICAL CENTER · PI LEE, PENG · 2014 to 2014
–
BLRD VA I01 BX001505NCI NIH HHS 1U01CA149556-01NCI NIH HHS P30 CA016087NCI NIH HHS T32 CA009161NCI NIH HHS U01 CA149556NCRR NIH HHS 1UL1RR029893NCRR NIH HHS UL1 RR029893
6 · The paper itself

Abstract

Androgen receptor (AR), a steroid hormone receptor, is critical for prostate cancer growth. However, activation of AR by androgens can also lead to growth suppression and differentiation. Transcriptional cofactors play an important role in this switch between proliferative and anti-proliferative AR target gene programs. Transducin β-like-related protein 1 (TBLR1), a core component of the nuclear receptor corepressor complex, shows both corepressor and coactivator activities on nuclear receptors, but little is known about its effects on AR and prostate cancer. We characterized TBLR1 as a coactivator of AR in prostate cancer cells and determined that the activation is dependent on both phosphorylation and 19S proteosome. We showed that TBLR1 physically interacts with AR and directly occupies the androgen-response elements of the affected AR target genes in an androgen-dependent manner. TBLR1 is primarily localized in the nucleus in benign prostate cells and nuclear expression is significantly reduced in prostate cancer cells in culture. Similarly, in human tumor samples, the expression of TBLR1 in the nucleus is significantly reduced in the malignant glands compared with the surrounding benign prostatic glands (P<0.005). Stable ectopic expression of nuclear TBLR1 leads to androgen-dependent growth suppression of prostate cancer cells in vitro and in vivo by selective activation of androgen-regulated genes associated with differentiation (e.g. KRT18) and growth suppression (e.g. NKX3-1), but not cell proliferation of the prostate cancer. Understanding the molecular switches involved in the transition from AR-dependent growth promotion to AR-dependent growth suppression will lead to more successful treatments for prostate cancer.

Indexed as

AdenocarcinomaAnimalsCell Growth ProcessesCell Line, TumorChromatin ImmunoprecipitationHumansMaleMice, NudeNuclear ProteinsProstatic NeoplasmsReceptors, AndrogenReceptors, Cytoplasmic and NuclearRepressor ProteinsReverse Transcriptase Polymerase Chain ReactionRNA, NeoplasmTissue Array AnalysisAR protein, humanNuclear ProteinsReceptors, AndrogenReceptors, Cytoplasmic and NuclearRepressor ProteinsRNA, NeoplasmTBL1XR1 protein, humanandrogenandrogen receptorgene expressiongene transcriptionprostate

Identifiers

PMID24243687
PMCPMC3947037
OpenAlexW2125346129

What OpenQuestion holds

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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.