Evidence map›Paper›PMID 21266977›Full record

ArticleBritish journal of cancer2011

ERK5 signalling in prostate cancer promotes an invasive phenotype.

A K Ramsay, S R C McCracken, M Soofi, J Fleming, A X Yu, I Ahmad, R Morland, L Machesky, C Nixon, D R Edwards and 5 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.3field-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

49 citing papers in PubMed, 90 citations in OpenAlex.

  1. MAPK ERK5 is a novel regulator of MHC-I in cancer cells.Cell communication and signaling : CCS · 2026
    Article
  2. The impact of dysregulation SUMOylation on prostate cancer.Journal of translational medicine · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. OXTRNature communications · 2022
    Article
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  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Impact of ERK5 on the Hallmarks of Cancer.International journal of molecular sciences · 2019
    Review
  20. Nuclear ERK: Mechanism of Translocation, Substrates, and Role in Cancer.International journal of molecular sciences · 2019
    Review
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

15 authors at 5 institutions in 1 country.

A K RamsayInstitute for Cancer Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G61 1BD, UK.
S R C McCracken
M Soofi
J Fleming
A X Yu
I Ahmad
R Morland
L Machesky
C Nixon
D R Edwards
R K Nuttall
M Seywright
R Marquez
E Keller
H Y Leung
Cancer Research UK Scotland Institute · GBUniversity of Glasgow · GBUniversity of East Anglia · GBNewcastle University · GBNHS Greater Glasgow and Clyde · GB

Funding

VACCINIA PSA FOR ANDROGEN-MODULATED POST-SURGICAL RECURRENCE OF PROSTATE CANCERP50CA069568 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COONEY, KATHLEEN A · 1995 to 2013
$31.3M
Cancer Research UKMedical Research Council G0802141Medical Research Council G0900871NCI NIH HHS P50 CA069568NCI NIH HHS P50CA69568.
6 · The paper itself

Abstract

backgroundAberrant mitogen/extracellular signal-regulated kinase 5 (MEK5)-extracellular signal-regulated protein kinase 5 (ERK5)-mediated signalling has been implicated in a number of tumour types including prostate cancer (PCa). The molecular basis of ERK5-driven carcinogenesis and its clinical relevance remain to be fully characterised.

methodsModulation of ERK5 expression or function in human PCa PC3 and PC3-ERK5 (stably transfected with ERK5) cells was performed using siRNA-mediated knockdown or the MEK inhibitor PD18435 respectively. In vitro significance of ERK5 signalling was assessed by assays for proliferation, motility, invasion and invadopodia. Expression of matrix metalloproteinases/tissue inhibitors of metalloproteases was determined by Q-RT-PCR. Extracellular signal-regulated protein kinase 5 expression in primary and metastatic PCa was examined using immunohistochemistry.

resultsReduction of ERK5 expression or signalling significantly inhibited the motility and invasive capability of PC3 cells. Extracellular signal-regulated protein kinase 5-mediated signalling significantly promoted formation of in vivo metastasis in an orthotopic PCa model (P<0.05). Invadopodia formation was also enhanced by forced ERK5 expression in PC3 cells. Furthermore, in metastatic PCa, nuclear ERK5 immunoreactivity was significantly upregulated when compared with benign prostatic hyperplasia and primary PCa (P=0.013 and P<0.0001, respectively).

conclusionOur in vitro, in vivo and clinical data support an important role for the MEK5-ERK5 signalling pathway in invasive PCa, which represents a potential target for therapy in primary and metastatic PCa.

Indexed as

AnimalsBenzamidesCell MovementCell ProliferationCells, CulturedDrug Evaluation, PreclinicalGene Expression Regulation, NeoplasticHumansMaleMAP Kinase Kinase 5MAP Kinase Signaling SystemMiceMice, NudeMitogen-Activated Protein Kinase 7Neoplasm InvasivenessPhenotype2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamideBenzamidesMAP2K5 protein, humanMAP Kinase Kinase 5Mitogen-Activated Protein Kinase 7Protein Kinase InhibitorsRNA, Small Interfering

Identifiers

PMID21266977
PMCPMC3049582
OpenAlexW2069981394

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.