Evidence map›Paper›PMID 27428423›Full record

ArticleEBioMedicine2016

Glycosylation is an Androgen-Regulated Process Essential for Prostate Cancer Cell Viability.

Jennifer Munkley, Daniel Vodak, Karen E Livermore, Katherine James, Brian T Wilson, Bridget Knight, Paul Mccullagh, John Mcgrath, Malcolm Crundwell, Lorna W Harries and 5 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. GalNAc-Transferases in Cancer.Biomedicines · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Glycosylation in Cancer.Handbook of experimental pharmacology · 2025
    Review
  14. Metabolic adaptations in prostate cancer.British journal of cancer · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

7 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

15 authors at 9 institutions in 2 countries.

Jennifer MunkleyInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne NE1 3BZ, UK. Electronic address: jennifer.munkley@ncl.ac.uk.
Daniel VodakBioinformatics Core Facility, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
Karen E LivermoreInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne NE1 3BZ, UK.
Katherine JamesInterdisciplinary Computing and Complex BioSystems Research Group, Newcastle University, Newcastle upon Tyne, UK.
Brian T WilsonInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne NE1 3BZ, UK; Northern Genetics Service, Newcastle Upon Tyne NHS Foundation Trust, International Centre for Life, Newcastle upon Tyne, UK.
Bridget KnightNIHR Exeter Clinical Research Facility, RD&E NHS Foundation Trust, UK.
Paul MccullaghDepartment of Pathology, RD&E NHS Foundation Trust, UK.
John McgrathExeter Surgical Health Services Research Unit, RD&E NHS Foundation Trust, UK.
Malcolm CrundwellDepartment of Urology, Royal Devon and Exeter NHS Foundation Trust, Exeter, UK.
Lorna W HarriesInstitute of Biomedical and Clinical Sciences, University of Exeter, Devon EX1 2LU, UK.
Hing Y LeungCancer Research UK Beatson Institute, Glasgow G61 1BD, UK; Institute of Cancer Sciences, University of Glasgow, Glasgow G12 8QQ, UK.
Craig N RobsonNorthern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
Ian G MillsProstate Cancer Research Group, Centre for Molecular Medicine Norway (NCMM), University of Oslo and Oslo University Hospitals, Oslo, Norway; Departments of Molecular Oncology, Institute of Cancer Research and Radium Hospital, Oslo, Norway; PCUK/Movember Centre of Excellence for Prostate Cancer Research, Centre for Cancer Research and Cell Biology (CCRCB), Queen's University, Belfast, UK.
Prabhakar RajanBarts Cancer Institute, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK.
David J ElliottInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne NE1 3BZ, UK.
Newcastle University · GBRoyal Devon & Exeter NHS Foundation Trust · GBCentre for Life · GBNIHR Exeter Clinical Research Facility · GBNorwegian Cancer Society · NOOslo University Hospital · NOQueen Mary University of London · GBUniversity of Exeter · GBUniversity of Glasgow · GB

Funding

Cancer Research UK 15339Prostate Cancer UK PG12-34
6 · The paper itself

Abstract

Steroid androgen hormones play a key role in the progression and treatment of prostate cancer, with androgen deprivation therapy being the first-line treatment used to control cancer growth. Here we apply a novel search strategy to identify androgen-regulated cellular pathways that may be clinically important in prostate cancer. Using RNASeq data, we searched for genes that showed reciprocal changes in expression in response to acute androgen stimulation in culture, and androgen deprivation in patients with prostate cancer. Amongst 700 genes displaying reciprocal expression patterns we observed a significant enrichment in the cellular process glycosylation. Of 31 reciprocally-regulated glycosylation enzymes, a set of 8 (GALNT7, ST6GalNAc1, GCNT1, UAP1, PGM3, CSGALNACT1, ST6GAL1 and EDEM3) were significantly up-regulated in clinical prostate carcinoma. Androgen exposure stimulated synthesis of glycan structures downstream of this core set of regulated enzymes including sialyl-Tn (sTn), sialyl Lewis(X) (SLe(X)), O-GlcNAc and chondroitin sulphate, suggesting androgen regulation of the core set of enzymes controls key steps in glycan synthesis. Expression of each of these enzymes also contributed to prostate cancer cell viability. This study identifies glycosylation as a global target for androgen control, and suggests loss of specific glycosylation enzymes might contribute to tumour regression following androgen depletion therapy.

Indexed as

Gene Expression Regulation, NeoplasticAndrogensCell Line, TumorCell SurvivalCluster AnalysisComputational BiologyDermatan SulfateGene Expression ProfilingGene Expression Regulation, EnzymologicGlycosylationHigh-Throughput Nucleotide SequencingHumansMaleProstatic NeoplasmsTranscriptomeAndrogensDermatan Sulfate

Identifiers

PMID27428423
PMCPMC4919605
OpenAlexW2341210755

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.