Evidence map›Paper›PMID 28382513›Full record

ReviewHuman genetics2017

RNA splicing and splicing regulator changes in prostate cancer pathology.

Jennifer Munkley, Karen Livermore, Prabhakar Rajan, David J Elliott

Abstract readReview
In one paragraph

Review in Human genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
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

43 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Increased ErbB2 Signaling Is an Early Adaptation to Androgen Signaling Inhibition and Persists in Castration-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Alternatively Spliced Isoforms ofJournal of personalized medicine · 2023
    Article
  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

4 authors.

Jennifer MunkleyInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle, NE1 3BZ, England, UK.
Karen LivermoreInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle, NE1 3BZ, England, UK.
Prabhakar RajanBarts Cancer Institute, John Vane Science Centre, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
David J ElliottInstitute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle, NE1 3BZ, England, UK. David.Elliott@ncl.ac.uk.

Funding

Prostate Cancer UK PG12-34Prostate Cancer UK S13-020
6 · The paper itself

Abstract

Changes in mRNA splice patterns have been associated with key pathological mechanisms in prostate cancer progression. The androgen receptor (abbreviated AR) transcription factor is a major driver of prostate cancer pathology and activated by androgen steroid hormones. Selection of alternative promoters by the activated AR can critically alter gene function by switching mRNA isoform production, including creating a pro-oncogenic isoform of the normally tumour suppressor gene TSC2. A number of androgen-regulated genes generate alternatively spliced mRNA isoforms, including a prostate-specific splice isoform of ST6GALNAC1 mRNA. ST6GALNAC1 encodes a sialyltransferase that catalyses the synthesis of the cancer-associated sTn antigen important for cell mobility. Genetic rearrangements occurring early in prostate cancer development place ERG oncogene expression under the control of the androgen-regulated TMPRSS2 promoter to hijack cell behaviour. This TMPRSS2-ERG fusion gene shows different patterns of alternative splicing in invasive versus localised prostate cancer. Alternative AR mRNA isoforms play a key role in the generation of prostate cancer drug resistance, by providing a mechanism through which prostate cancer cells can grow in limited serum androgen concentrations. A number of splicing regulator proteins change expression patterns in prostate cancer and may help drive key stages of disease progression. Up-regulation of SRRM4 establishes neuronal splicing patterns in neuroendocrine prostate cancer. The splicing regulators Sam68 and Tra2β increase expression in prostate cancer. The SR protein kinase SRPK1 that modulates the activity of SR proteins is up-regulated in prostate cancer and has already given encouraging results as a potential therapeutic target in mouse models.

Indexed as

Gene Expression Regulation, NeoplasticNeoplasm ProteinsRNA, MessengerRNA, NeoplasmRNA SplicingAdaptor Proteins, Signal TransducingAnimalsDNA-Binding ProteinsHumansMaleMiceNerve Tissue ProteinsProstatic NeoplasmsProtein Serine-Threonine KinasesRNA-Binding ProteinsSerine-Arginine Splicing FactorsAdaptor Proteins, Signal TransducingDNA-Binding ProteinsKHDRBS1 protein, humanKhdrbs1 protein, mouseNeoplasm ProteinsNerve Tissue ProteinsProtein Serine-Threonine KinasesRNA-Binding ProteinsRNA, MessengerRNA, NeoplasmSerine-Arginine Splicing FactorsSRPK1 protein, humanSrpk1 protein, mouseSRRM4 protein, humanTRA2B protein, humanTra2b protein, mouseAbirateroneAndrogen Deprivation TherapyAndrogen ReceptorProstate CancerProstate Cancer Cell

Identifiers

PMID28382513
PMCPMC5602090

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.