Evidence map›Paper›PMID 28006818›Full record

ArticleBritish journal of cancer2017

Tumour-derived alkaline phosphatase regulates tumour growth, epithelial plasticity and disease-free survival in metastatic prostate cancer.

S R Rao, A E Snaith, D Marino, X Cheng, S T Lwin, I R Orriss, F C Hamdy, C M Edwards

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 3 pooled it
9.7field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 3 syntheses or guidelines pooled it, 185 citations in OpenAlex.

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  17. Ectonucleotidases and purinergic receptors in mouse prostate gland.American journal of clinical and experimental urology · 2025
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21 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

8 authors at 3 institutions in 1 country.

S R RaoNuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 7LD, UK.
A E SnaithNuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 7LD, UK.
D MarinoNuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 7LD, UK.
X ChengNuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 7LD, UK.
S T LwinNuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 7LD, UK.
I R OrrissRoyal Veterinary College, University of London, London NW1 0TU, UK.
F C HamdyNuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 7LD, UK.
C M EdwardsNuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 7LD, UK.
University of Oxford · GBNuffield Orthopaedic Centre · GBUniversity of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent evidence suggests that bone-related parameters are the main prognostic factors for overall survival in advanced prostate cancer (PCa), with elevated circulating levels of alkaline phosphatase (ALP) thought to reflect the dysregulated bone formation accompanying distant metastases. We have identified that PCa cells express ALPL, the gene that encodes for tissue nonspecific ALP, and hypothesised that tumour-derived ALPL may contribute to disease progression.

methodsFunctional effects of ALPL inhibition were investigated in metastatic PCa cell lines. ALPL gene expression was analysed from published PCa data sets, and correlated with disease-free survival and metastasis.

resultsALPL expression was increased in PCa cells from metastatic sites. A reduction in tumour-derived ALPL expression or ALP activity increased cell death, mesenchymal-to-epithelial transition and reduced migration. Alkaline phosphatase activity was decreased by the EMT repressor Snail. In men with PCa, tumour-derived ALPL correlated with EMT markers, and high ALPL expression was associated with a significant reduction in disease-free survival.

conclusionsOur studies reveal the function of tumour-derived ALPL in regulating cell death and epithelial plasticity, and demonstrate a strong association between ALPL expression in PCa cells and metastasis or disease-free survival, thus identifying tumour-derived ALPL as a major contributor to the pathogenesis of PCa progression.

Indexed as

Alkaline PhosphataseAnimalsCell DeathCell MovementCell ProliferationCells, CulturedDisease-Free SurvivalDisease ProgressionEpithelial-Mesenchymal TransitionHEK293 CellsHumansMaleMiceNeoplasm MetastasisProstatic NeoplasmsAlkaline Phosphatase

Identifiers

PMID28006818
PMCPMC5243990
OpenAlexW2562047649

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.