Evidence map›Paper›PMID 25341046›Full record

ArticleCell death & disease2014

Nuclear iASPP may facilitate prostate cancer progression.

E V Morris, L Cerundolo, M Lu, C Verrill, F Fritzsche, M J White, G N Thalmann, C S ten Donkelaar, I Ratnayaka, V Salter and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Overexpression of iASPP-SV in glioma is associated with poor prognosis by promoting cell viability and antagonizing apoptosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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 4 institutions in 3 countries.

E V Morris1] Ludwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK [2] Nuffield Department of Surgical Sciences, University of Oxford, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
L Cerundolo1] Ludwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK [2] Nuffield Department of Surgical Sciences, University of Oxford, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
M LuLudwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
C VerrillDepartment of Cellular Pathology and NIHR Oxford Biomedical Research Centre, Oxford University Hospitals NHS Trust, John Radcliffe Hospital, Headley Way, Oxford, UK.
F FritzscheLudwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
M J WhiteLudwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
G N ThalmannDepartment of Urology, Inselspital, Bern, Switzerland.
C S ten DonkelaarLudwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
I RatnayakaLudwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
V SalterLudwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
F C HamdyNuffield Department of Surgical Sciences, University of Oxford, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
X LuLudwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
R J Bryant1] Ludwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK [2] Nuffield Department of Surgical Sciences, University of Oxford, Old Road Campus Research Building (off Roosevelt Drive), Headington, Oxford, UK.
Ludwig Cancer Research · BEOxford University Hospitals NHS Trust · GBUniversity Hospital of Bern · CHUniversity of Oxford · GB

Funding

Medical Research Council
6 · The paper itself

Abstract

One of the major challenges in prostate cancer (PCa) research is the identification of key players that control the progression of primary cancers to invasive and metastatic disease. The majority of metastatic PCa express wild-type p53, whereas loss of p63 expression, a p53 family member, is a common event. Here we identify inhibitor of apoptosis-stimulating protein of p53 (iASPP), a common cellular regulator of p53 and p63, as an important player of PCa progression. Detailed analysis of the prostate epithelium of iASPP transgenic mice, iASPP(Δ8/Δ8) mice, revealed that iASPP deficiency resulted in a reduction in the number of p63 expressing basal epithelial cells compared with that seen in wild-type mice. Nuclear and cytoplasmic iASPP expression was greater in PCa samples compared with benign epithelium. Importantly nuclear iASPP associated with p53 accumulation in vitro and in vivo. A pair of isogenic primary and metastatic PCa cell lines revealed that nuclear iASPP is enriched in the highly metastatic PCa cells. Nuclear iASPP is often detected in PCa cells located at the invasive leading edge in vivo. Increased iASPP expression associated with metastatic disease and PCa-specific death in a clinical cohort with long-term follow-up. These results suggest that iASPP function is required to maintain the expression of p63 in normal basal prostate epithelium, and nuclear iASPP may inactivate p53 function and facilitate PCa progression. Thus iASPP expression may act as a predictive marker of PCa progression.

Indexed as

Disease ProgressionAdultAgedAnimalsBiomarkers, TumorCell DifferentiationCell Line, TumorCell NucleusCoculture TechniquesCohort StudiesEpitheliumHumansIntracellular Signaling Peptides and ProteinsMaleMiceMiddle AgedBiomarkers, TumorIntracellular Signaling Peptides and ProteinsPPP1R13L protein, humanPpp1r13l protein, mouseRepressor ProteinsTumor Suppressor Proteins

Identifiers

PMID25341046
PMCPMC4649527
OpenAlexW1990679998

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.