Evidence map›Paper›PMID 26549027›Full record

ArticleOncogene2016

Cytoplasmic PML promotes TGF-β-associated epithelial-mesenchymal transition and invasion in prostate cancer.

M E Buczek, A K Miles, W Green, C Johnson, D J Boocock, A G Pockley, R C Rees, G Hulman, G van Schalkwyk, R Parkinson and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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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 3 institutions in 1 country.

M E BuczekJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, UK.
A K MilesJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, UK.
W GreenDepartment of Urology, City Hospital, Nottingham University Hospitals NHS Trust, Nottingham, UK.
C JohnsonJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, UK.
D J BoocockJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, UK.
A G PockleyJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, UK.
R C ReesJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, UK.
G HulmanDepartment of Cellular Pathology, Queen's Medical Centre, Nottingham University Hospitals Trust, Nottingham, UK.
G van SchalkwykDepartment of Histopathology, Royal Derby Hospital, Derby, UK.
R ParkinsonDepartment of Urology, City Hospital, Nottingham University Hospitals NHS Trust, Nottingham, UK.
J HulmanDepartment of Cellular Pathology, Queen's Medical Centre, Nottingham University Hospitals Trust, Nottingham, UK.
D G PoweJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, UK.
T RegadJohn van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, Nottingham, UK.
Nottingham Trent University · GBNottingham University Hospitals NHS Trust · GBRoyal Derby Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a key event that is involved in the invasion and dissemination of cancer cells. Although typically considered as having tumour-suppressive properties, transforming growth factor (TGF)-β signalling is altered during cancer and has been associated with the invasion of cancer cells and metastasis. In this study, we report a previously unknown role for the cytoplasmic promyelocytic leukaemia (cPML) tumour suppressor in TGF-β signalling-induced regulation of prostate cancer-associated EMT and invasion. We demonstrate that cPML promotes a mesenchymal phenotype and increases the invasiveness of prostate cancer cells. This event is associated with activation of TGF-β canonical signalling pathway through the induction of Sma and Mad related family 2 and 3 (SMAD2 and SMAD3) phosphorylation. Furthermore, the cytoplasmic localization of promyelocytic leukaemia (PML) is mediated by its nuclear export in a chromosomal maintenance 1 (CRM1)-dependent manner. This was clinically tested in prostate cancer tissue and shown that cytoplasmic PML and CRM1 co-expression correlates with reduced disease-specific survival. In summary, we provide evidence of dysfunctional TGF-β signalling occurring at an early stage in prostate cancer. We show that this disease pathway is mediated by cPML and CRM1 and results in a more aggressive cancer cell phenotype. We propose that the targeting of this pathway could be therapeutically exploited for clinical benefit.

Indexed as

Epithelial-Mesenchymal TransitionActive Transport, Cell NucleusCell Line, TumorCell MovementCell NucleusCytoplasmExportin 1 ProteinHumansImmunoblottingKaplan-Meier EstimateKaryopherinsMaleNeoplasm InvasivenessPhosphorylationPromyelocytic Leukemia ProteinProstatic NeoplasmsExportin 1 ProteinKaryopherinsPML protein, humanPromyelocytic Leukemia ProteinProtein Serine-Threonine KinasesReceptors, Cytoplasmic and NuclearReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISmad2 ProteinSMAD2 protein, humanSmad3 ProteinTransforming Growth Factor beta

Identifiers

PMID26549027
PMCPMC4932557
OpenAlexW2233631376

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.