Evidence map›Paper›PMID 26968201›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016

Nuclear Receptor Corepressor 1 Expression and Output Declines with Prostate Cancer Progression.

Sandra M Lopez, Alexander I Agoulnik, Manqi Zhang, Leif E Peterson, Egla Suarez, Gregory A Gandarillas, Anna Frolov, Rile Li, Kimal Rajapakshe, Christian Coarfa and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. SPEN inactivation drives resistance to androgen receptor pathway inhibitors in metastatic prostate cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  2. Deep Sequencing Reveals Novel Mutations inInternational journal of molecular sciences · 2025
    Article
  3. Functional inversion of circadian regulator REV-ERBα leads to tumorigenic gene reprogramming.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  7. Epigenetic Coregulation of Androgen Receptor Signaling.Advances in experimental medicine and biology · 2022
    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

13 authors at 1 institution in 1 country.

Sandra M LopezDepartment of Cellular Biology and Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida. Johns Hopkins University School of Medicine, Baltimore, Maryland.
Alexander I AgoulnikDepartment of Human and Molecular Genetics, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida. Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas.
Manqi ZhangDepartment of Cellular Biology and Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida.
Leif E PetersonCenter for Biostatistics, Houston Methodist Research Institute, Houston, Texas.
Egla SuarezDepartment of Cellular Biology and Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida.
Gregory A GandarillasDepartment of Cellular Biology and Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida.
Anna FrolovDan L. Duncan Cancer Center-Biostatistics, Baylor College of Medicine, Houston, Texas.
Rile LiDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, Texas.
Kimal RajapaksheDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Christian CoarfaDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Michael M IttmannDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, Texas. Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas.
Nancy L WeigelDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.
Irina U AgoulnikDepartment of Cellular Biology and Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas. Biomolecular Sciences Institute, School of Integrated Science and Humanity, Florida international University, Miami, Florida. Irina.Agoulnik@fiu.edu.
Baylor College of Medicine · US

Funding

Regulation of metastases by tumor suppressor INPP4BR15CA179287 · NCI · FLORIDA INTERNATIONAL UNIVERSITY · PI AGOULNIK, IRINA · 2014 to 2014
$418k
Role of NCoR in Antiandrogen Resistance in Prostate CancerR21CA129265 · NCI · FLORIDA INTERNATIONAL UNIVERSITY · PI AGOULNIK, IRINA · 2008 to 2009
$380k
NCI NIH HHS R15 CA179287NCI NIH HHS R21 CA129265
6 · The paper itself

Abstract

purposeCastration therapy in advanced prostate cancer eventually fails and leads to the development of castration-resistant prostate cancer (CRPC), which has no cure. Characteristic features of CRPC can be increased androgen receptor (AR) expression and altered transcriptional output. We investigated the expression of nuclear receptor corepressor 1 (NCOR1) in human prostate and prostate cancer and the role of NCOR1 in response to antiandrogens. EXPERIMENTAL

designNCOR1 protein levels were compared between matched normal prostate and prostate cancer in 409 patient samples. NCOR1 knockdown was used to investigate its effect on bicalutamide response in androgen-dependent prostate cancer cell lines and transcriptional changes associated with the loss of NCOR1. NCOR1 transcriptional signature was also examined in prostate cancer gene expression datasets.

resultsNCOR1 protein was detected in cytoplasm and nuclei of secretory epithelial cells in normal prostate. Both cytoplasmic and nuclear NCOR1 protein levels were lower in prostate cancer than in normal prostate. Prostate cancer metastases show significant decrease in NCOR1 transcriptional output. Inhibition of LNCaP cellular proliferation by bicalutamide requires NCOR1. NCOR1-regulated genes suppress cellular proliferation and mediate bicalutamide resistance. In the mouse, NCOR1 is required for bicalutamide-dependent regulation of a subset of the AR target genes.

conclusionsIn summary, we demonstrated that NCOR1 function declines with prostate cancer progression. Reduction in NCOR1 levels causes bicalutamide resistance in LNCaP cells and compromises response to bicalutamide in mouse prostate in vivo Clin Cancer Res; 22(15); 3937-49. ©2016 AACR.

Indexed as

Gene ExpressionAndrogen AntagonistsAndrogensAnilidesAnimalsCell Line, TumorDisease Models, AnimalDisease ProgressionGene Knockdown TechniquesGene SilencingHumansMaleMiceMice, TransgenicNeoplasm MetastasisNitrilesAndrogen AntagonistsAndrogensAnilidesbicalutamideNCOR1 protein, humanNitrilesNuclear Receptor Co-Repressor 1Tosyl Compounds

Identifiers

PMID26968201
PMCPMC4970919
OpenAlexW2293257570

What OpenQuestion holds

Textmetadata
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.