Evidence map›Paper›PMID 24240687›Full record

ArticleOncogene2014

N-acetyl-L-aspartyl-L-glutamate peptidase-like 2 is overexpressed in cancer and promotes a pro-migratory and pro-metastatic phenotype.

H C Whitaker, L L Shiong, J D Kay, H Grönberg, A Y Warren, A Seipel, F Wiklund, B Thomas, P Wiklund, J L Miller and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 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, 38 citations in OpenAlex.

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  8. Observational
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  16. Comparison ofOncotarget · 2017
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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

16 authors at 5 institutions in 2 countries.

H C Whitaker1] Uro-Oncology Research Group, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK [2] Cancer Research UK Biomarker Initiative, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
L L ShiongUro-Oncology Research Group, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
J D KayUro-Oncology Research Group, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
H GrönbergDepartment of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
A Y Warren1] Department of Histopathology and ISH Core Facility, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK [2] Department of Histopathology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
A SeipelDepartment of Pathology, Karolinska Institute, Stockholm, Sweden.
F WiklundDepartment of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
B ThomasUro-Oncology Research Group, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
P WiklundDepartment of Pathology, Karolinska Institute, Stockholm, Sweden.
J L Miller1] Department of Histopathology and ISH Core Facility, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK [2] Department of Histopathology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
S MenonBioinformatics Core Facility, Cancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK.
A Ramos-MontoyaUro-Oncology Research Group, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
S L VowlerBioinformatics Core Facility, Cancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge, UK.
C MassieUro-Oncology Research Group, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
L EgevadDepartment of Pathology, Karolinska Institute, Stockholm, Sweden.
D E NealUro-Oncology Research Group, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK.
Karolinska Institutet · SEUniversity of Cambridge · GBCancer Research UK Cambridge Center · GBCambridge University Hospitals NHS Foundation Trust · GBCancer Research UK · GB

Funding

Medical Research Council G0500966Medical Research Council G0900871Prostate Cancer UK G2012/50
6 · The paper itself

Abstract

N-acetyl-L-aspartyl-L-glutamate peptidase-like 2 (NAALADL2) is a member of the glutamate carboxypeptidase II family, best characterized by prostate-specific membrane antigen (PSMA/NAALAD1). Using immunohistochemistry (IHC), we have shown overexpression of NAALADL2 in colon and prostate tumours when compared with benign tissue. In prostate cancer, NAALADL2 expression was associated with stage and Grade, as well as circulating mRNA levels of the NAALADL2 gene. Overexpression of NAALADL2 was shown to predict poor survival following radical prostatectomy. In contrast to PSMA/NAALAD1, NAALADL2 was localized at the basal cell surface where it promotes adhesion to extracellular matrix proteins. Using stable knockdown and overexpression cell lines, we have demonstrated NAALADL2-dependent changes in cell migration, invasion and colony-forming potential. Expression arrays of the knockdown and overexpression cell lines have identified nine genes that co-expressed with NAALADL2, which included membrane proteins and genes known to be androgen regulated, including the prostate cancer biomarkers AGR2 and SPON2. Androgen regulation was confirmed in a number of these genes, although NAALADL2 itself was not found to be androgen regulated. NAALADL2 was also found to regulate levels of Ser133 phosphorylated C-AMP-binding protein (CREB), a master regulator of a number of cellular processes involved in cancer development and progression. In combination, these data suggest that changes in expression of NAALADL2 can impact upon a number of pro-oncogenic pathways and processes, making it a useful biomarker for both diagnosis and prognosis.

Indexed as

Gene Expression Regulation, NeoplasticAntigens, SurfaceBiomarkers, TumorBlotting, WesternCell Line, TumorCell MovementFollow-Up StudiesGene Expression ProfilingGlutamate Carboxypeptidase IIHumansImmunohistochemistryKaplan-Meier EstimateMaleMicroscopy, ConfocalNeoplasm GradingNeoplasm MetastasisAntigens, SurfaceBiomarkers, TumorFOLH1 protein, humanGlutamate Carboxypeptidase IINAALADL2 protein, human

Identifiers

PMID24240687
OpenAlexW2075796770

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.