Evidence map›Paper›PMID 27760327›Full record

ArticleCell reports2016

Androgen Receptor Tumor Suppressor Function Is Mediated by Recruitment of Retinoblastoma Protein.

Shuai Gao, Yanfei Gao, Housheng Hansen He, Dong Han, Wanting Han, Amy Avery, Jill A Macoska, Xiaming Liu, Sen Chen, Fen Ma and 3 more

Abstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
–field-weighted citation impact
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

65 citing papers in PubMed.

  1. Lack of synergy between AR-targeted therapies and PARP inhibitors in homologous recombination-proficient prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
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5 more citing papers are in PubMed but not listed here.

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

13 authors.

Shuai GaoCenter for Personalized Cancer Therapy, University of Massachusetts, Boston, Boston, MA 02125, USA; Hematology-Oncology Division and Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Yanfei GaoHematology-Oncology Division and Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA; Department of Orthopedics, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.
Housheng Hansen HeOntario Cancer Institute, Princess Margaret Cancer Center/University Health Network, Toronto, ON M5G1L7, Canada.
Dong HanCenter for Personalized Cancer Therapy, University of Massachusetts, Boston, Boston, MA 02125, USA.
Wanting HanCenter for Personalized Cancer Therapy, University of Massachusetts, Boston, Boston, MA 02125, USA.
Amy AveryCenter for Personalized Cancer Therapy, University of Massachusetts, Boston, Boston, MA 02125, USA.
Jill A MacoskaCenter for Personalized Cancer Therapy, University of Massachusetts, Boston, Boston, MA 02125, USA.
Xiaming LiuDepartment of Urology, Tongji Hospital, Wuhan, Hubei 430030, China.
Sen ChenHematology-Oncology Division and Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Fen MaHematology-Oncology Division and Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Shaoyong ChenHematology-Oncology Division and Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. Electronic address: schen@bidmc.harvard.edu.
Steven P BalkHematology-Oncology Division and Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. Electronic address: sbalk@bidmc.harvard.edu.
Changmeng CaiCenter for Personalized Cancer Therapy, University of Massachusetts, Boston, Boston, MA 02125, USA; Hematology-Oncology Division and Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. Electronic address: changmeng.cai@umb.edu.

Funding

Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI LODA, MASSIMO · 2002 to 2017
$36.2M
Steroid Metabolism in Castration-Resistant Prostate CancerP01CA163227 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Henry W. Long · 2013 to 2026
$25.0M
Molecular basis of androgen receptor mediated gene transcriptional repressionR00CA166507 · NCI · UNIVERSITY OF MASSACHUSETTS BOSTON · PI CAI, CHANGMENG · 2015 to 2017
$726k
Androgen Receptor Regulation by PhosphorylationR00CA135592 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CHEN, SHAOYONG · 2011 to 2013
$710k
Molecular basis of androgen receptor mediated gene transcriptional repressionK99CA166507 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CAI, CHANGMENG · 2012 to 2013
$270k
Epigenetic Regulators in Cancer Development and ProgressionK99CA172948 · NCI · DANA-FARBER CANCER INST · PI HE, HOUSHENG · 2013 to 2013
$63k
NCI NIH HHS K99 CA166507NCI NIH HHS K99 CA172948NCI NIH HHS P01 CA163227NCI NIH HHS P50 CA090381NCI NIH HHS R00 CA135592NCI NIH HHS R00 CA166507
6 · The paper itself

Abstract

Although well characterized as a transcriptional activator that drives prostate cancer (PCa) growth, androgen receptor (AR) can function as a transcriptional repressor, and high-level androgens can suppress PCa proliferation. The molecular basis for this repression activity remains to be determined. Genes required for DNA replication are highly enriched among androgen-repressed genes, and AR is recruited to the majority of these genes, where it rapidly represses their transcription. This activity is enhanced in PCa cells expressing high AR levels and is mediated by recruitment of hypophosphorylated retinoblastoma protein (Rb). Significantly, AR also indirectly increases the expression of DNA replication genes through stimulatory effects on other metabolic genes with subsequent CDK activation and Rb hyperphosphorylation. In castration-resistant PCa cells, which are dependent on high-level AR expression, this anti-proliferative repression function might be exploited through treatment with androgen in combination with agents that suppress AR-driven metabolic functions or cell cycle progression.

Indexed as

Genes, Tumor SuppressorAndrogensCell Line, TumorCell ProliferationCyclin-Dependent KinasesDNA ReplicationGene Expression Regulation, NeoplasticHumansMaleProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantReceptors, AndrogenRetinoblastoma ProteinTranscription, GeneticAndrogensAR protein, humanCyclin-Dependent KinasesReceptors, AndrogenRetinoblastoma Proteinandrogen deprivation therapyandrogen receptorARDNA damage repairDNA replicationE2F1metabolismprostate cancerRbRetinoblastoma proteintranscriptional repression

Identifiers

PMID27760327
PMCPMC5123835

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.