Evidence map›Paper›PMID 22349817›Full record

ArticleOncogene2013

Increased expression of NuSAP in recurrent prostate cancer is mediated by E2F1.

Z G Gulzar, J K McKenney, J D Brooks

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Targeting AXL Inhibits the Growth and Metastasis of Prostate Cancer in Bone.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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24 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

3 authors at 1 institution in 1 country.

Z G GulzarDepartment of Urology, Stanford University School of Medicine, Stanford, CA 94305-5118, USA.
J K McKenney
J D Brooks
Stanford University · US

Funding

Gene Amplification and Deletion in Pancreatic CancerR01CA112016 · NCI · STANFORD UNIVERSITY · PI POLLACK, JONATHAN R · 2006 to 2010
$1.4M
Translating Prostate Cancer Gene Expression SubtypesR01CA111782 · NCI · STANFORD UNIVERSITY · PI BROOKS, JAMES D. · 2005 to 2008
$1.1M
Identifying the tumor suppressor gene at 6q15 indolent prostate cancerF32CA130472 · NCI · STANFORD UNIVERSITY · PI HUANG, STEPHANIE · 2008 to 2011
$157k
NCI NIH HHS CA111782NCI NIH HHS CA112016NCI NIH HHS CA130472NCI NIH HHS F32 CA130472NCI NIH HHS R01 CA111782NCI NIH HHS R01 CA112016
6 · The paper itself

Abstract

Increasing evidence suggests that prostate cancer is overdiagnosed and overtreated, and prognostic biomarkers would aid in treatment selection. To define prognostic biomarkers for aggressive prostate cancer, we carried out gene-expression profiling of 98 prostate tumors and 52 benign adjacent prostate tissue samples with detailed clinical annotation. We identified 28 transcripts significantly associated with recurrence after radical prostatectomy including NuSAP, a protein that binds DNA to the mitotic spindle. Elevated NuSAP transcript levels were associated with poor outcome in two independent prostate cancer gene-expression datasets. To characterize the role and regulation of NuSAP in prostate cancer, we studied the expression of NuSAP in the LNCaP and PC3 human prostate cancer cell lines. Posttranscriptional silencing of the NuSAP gene severely hampered the ability of PC3 to invade and proliferate in vitro. The promoter region of the NuSAP gene contains two CCAAT boxes and binding sites for E2F. Transient transfection of an E2F1 cDNA and 431 bp of the NuSAP promoter demonstrated E2F1 as an important regulator of expression. Deletion of the E2F-binding site at nucleotide -246 negated the effects of E2F1 on NuSAP expression. Electrophoretic mobility shift assays demonstrated that nuclear extracts of cells overexpressing E2F1 bound directly to the E2F-binding site in the NuSAP promoter region. Finally, immunohistochemistry showed a strong correlation between E2F1 and NuSAP expression in human prostate cancer samples. NuSAP is a novel biomarker for prostate cancer recurrence after surgery and its overexpression appears to be driven in part by E2F1 activation.

Indexed as

Base SequenceCell Line, TumorDNA, ComplementaryE2F1 Transcription FactorElectrophoretic Mobility Shift AssayGene Expression ProfilingHumansImmunohistochemistryMaleMicrotubule-Associated ProteinsMolecular Sequence DataPromoter Regions, GeneticProstatic NeoplasmsRecurrenceRNA, MessengerDNA, ComplementaryE2F1 protein, humanE2F1 Transcription FactorMicrotubule-Associated ProteinsNUSAP1 protein, humanRNA, Messenger

Identifiers

PMID22349817
PMCPMC3360134
OpenAlexW2083003255

What OpenQuestion holds

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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.