Evidence map›Paper›PMID 25592066›Full record

ArticleBMC cancer2015

Androgen-regulation of the protein tyrosine phosphatase PTPRR activates ERK1/2 signalling in prostate cancer cells.

Jennifer Munkley, Nicholas P Lafferty, Gabriela Kalna, Craig N Robson, Hing Y Leung, Prabhakar Rajan, David J Elliott

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. [Risk modeling based on HER-2 related genes for bladder cancer survival prognosis assessment].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023
    Article
  9. Article
  10. Review
  11. Article
  12. Molecules (Basel, Switzerland) · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

7 authors at 2 institutions in 1 country.

Jennifer MunkleyInstitute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, NE1 3BZ, UK. jennifer.munkley@ncl.ac.uk.
Nicholas P LaffertyInstitute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, NE1 3BZ, UK. n.p.lafferty@gmail.com.
Gabriela KalnaCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK. g.kalna@beatson.gla.ac.uk.
Craig N RobsonNorthern Institute for Cancer Research, Newcastle University, Newcastle-upon-Tyne, NE2 4HH, UK. c.n.robson@ncl.ac.uk.
Hing Y LeungCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK. Hing.Leung@glasgow.ac.uk.
Prabhakar RajanCancer Research UK Beatson Institute, Glasgow, G61 1BD, UK. Prabhakar.Rajan@glasgow.ac.uk.
David J ElliottInstitute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, NE1 3BZ, UK. david.elliott@ncl.ac.uk.
Newcastle University · GBCancer Research UK Scotland Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BB/1006923/1Cancer Research UK 15151Cancer Research UK 15339Prostate Cancer UK PG12-24Prostate Cancer UK PG12-34Prostate Cancer UK S12-018Wellcome Trust WT080368MAWellcome Trust WT089225/Z/09/Z
6 · The paper itself

Abstract

backgroundAndrogens drive the onset and progression of prostate cancer (PCa) via androgen receptor (AR) signalling. The principal treatment for PCa is androgen deprivation therapy, although the majority of patients eventually develop a lethal castrate-resistant form of the disease, where despite low serum testosterone levels AR signalling persists. Advanced PCa often has hyper-activated RAS/ERK1/2 signalling thought to be due to loss of function of key negative regulators of the pathway, the details of which are not fully understood.

methodsWe recently carried out a genome-wide study and identified a subset of 226 novel androgen-regulated genes (PLOS ONE 6:e29088, 2011). In this study we have meta-analysed this dataset with genes and pathways frequently mutated in PCa to identify androgen-responsive regulators of the RAS/ERK1/2 pathway.

resultsWe find the PTGER4 and TSPYL2 genes are up-regulated by androgen stimulation and the ADCY1, OPKR1, TRIB1, SPRY1 and PTPRR are down-regulated by androgens. Further characterisation of PTPRR protein in LNCaP cells revealed it is an early and direct target of the androgen receptor which negatively regulates the RAS/ERK1/2 pathway and reduces cell proliferation in response to androgens.

conclusionOur data suggest that loss of PTPRR in clinical PCa is one factor that might contribute to activation of the RAS/ERK1/2 pathway.

Indexed as

AndrogensCell Line, TumorCell ProliferationDatabases, GeneticGene Expression Regulation, NeoplasticHumansMaleMAP Kinase Signaling SystemProstatic NeoplasmsReceptor-Like Protein Tyrosine Phosphatases, Class 7Receptors, AndrogenAndrogensAR protein, humanPTPRR protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 7Receptors, Androgen

Identifiers

PMID25592066
PMCPMC4302442
OpenAlexW1967251048

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.