Evidence map›Paper›PMID 19223505›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009

Tumor suppressor BRCA1 is expressed in prostate cancer and controls insulin-like growth factor I receptor (IGF-IR) gene transcription in an androgen receptor-dependent manner.

Hagit Schayek, Kathy Haugk, Shihua Sun, Lawrence D True, Stephen R Plymate, Haim Werner

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

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  6. BRCA1: An Endocrine and Metabolic Regulator.Frontiers in endocrinology · 2022
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  12. Health effects associated with occupational exposure to hand-arm or whole body vibration.Journal of toxicology and environmental health. Part B, Critical reviews · 2018
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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

6 authors at 2 institutions in 2 countries.

Hagit SchayekDepartment of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Kathy Haugk
Shihua Sun
Lawrence D True
Stephen R Plymate
Haim Werner
University of Puget Sound · USTel Aviv University · IL

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI RUTH D ETZIONI · 2002 to 2026
$58.1M
NCI NIH HHS CA97186-06NCI NIH HHS P50 CA097186
6 · The paper itself

Abstract

purposeThe insulin-like growth factor (IGF) system plays an important role in prostate cancer. The BRCA1 gene encodes a transcription factor with tumor suppressor activity. The involvement of BRCA1 in prostate cancer, however, has not yet been elucidated. The purpose of the present study was to examine the functional correlations between BRCA1 and the IGF system in prostate cancer. EXPERIMENTAL

designAn immunohistochemical analysis of BRCA1 was done on tissue microarrays comprising 203 primary prostate cancer specimens. In addition, BRCA1 levels were measured in prostate cancer xenografts and in cell lines representing early stages (P69 cells) and advanced stages (M12 cells) of the disease. The ability of BRCA1 to regulate IGF-I receptor (IGF-IR) expression was studied by coexpression experiments using a BRCA1 expression vector along with an IGF-IR promoter-luciferase reporter.

resultsWe found significantly elevated BRCA1 levels in prostate cancer in comparison with histologically normal prostate tissue (P<0.001). In addition, an inverse correlation between BRCA1 and IGF-IR levels was observed in the androgen receptor (AR)-negative prostate cancer-derived P69 and M12 cell lines. Coexpression experiments in M12 cells revealed that BRCA1 was able to suppress IGF-IR promoter activity and endogenous IGF-IR levels. On the other hand, BRCA1 enhanced IGF-IR levels in LNCaP C4-2 cells expressing an endogenous AR.

conclusionsWe provide evidence that BRCA1 differentially regulates IGF-IR expression in AR-positive and AR-negative prostate cancer cells. The mechanism of action of BRCA1 involves modulation of IGF-IR gene transcription. In addition, immunohistochemical data are consistent with a potential survival role of BRCA1 in prostate cancer.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticAgedAnimalsBlotting, WesternBRCA1 ProteinCell ProliferationHumansMaleMiceMice, NudeMiddle AgedPromoter Regions, GeneticProstateProstatic NeoplasmsReceptor, IGF Type 1AR protein, humanBRCA1 ProteinBRCA1 protein, humanReceptor, IGF Type 1Receptors, Androgen

Identifiers

PMID19223505
PMCPMC2935172
OpenAlexW2169443052

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.