Evidence map›Paper›PMID 25241896›Full record

ArticleOncogene2015

UAP1 is overexpressed in prostate cancer and is protective against inhibitors of N-linked glycosylation.

H M Itkonen, N Engedal, E Babaie, M Luhr, I J Guldvik, S Minner, J Hohloch, M C Tsourlakis, T Schlomm, I G Mills

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
2.8field-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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. NSUN2-mediated mTheranostics · 2025
    Article
  11. Metabolic adaptations in prostate cancer.British journal of cancer · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Pro-Survival Factor EDEM3 Confers Therapy Resistance in Prostate Cancer.International journal of molecular sciences · 2022
    Article

9 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

10 authors at 4 institutions in 2 countries.

H M ItkonenProstate Cancer Research Group, Centre for Molecular Medicine (Norway), University of Oslo and Oslo University Hospitals, Oslo, Norway.
N EngedalProstate Cancer Research Group, Centre for Molecular Medicine (Norway), University of Oslo and Oslo University Hospitals, Oslo, Norway.
E BabaieThe Biotechnology Center of Oslo, University of Oslo, Oslo, Norway.
M LuhrProstate Cancer Research Group, Centre for Molecular Medicine (Norway), University of Oslo and Oslo University Hospitals, Oslo, Norway.
I J GuldvikProstate Cancer Research Group, Centre for Molecular Medicine (Norway), University of Oslo and Oslo University Hospitals, Oslo, Norway.
S MinnerInstitute for Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
J HohlochInstitute for Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
M C TsourlakisInstitute for Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
T Schlomm1] Department of Urology, Section for translational Prostate Cancer Research University Medical Center Hamburg-Eppendorf, Hamburg, Germany [2] Martini Clinic, Prostate Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
I G Mills1] Prostate Cancer Research Group, Centre for Molecular Medicine (Norway), University of Oslo and Oslo University Hospitals, Oslo, Norway [2] Department of Cancer Prevention, Oslo University Hospitals, Oslo, Norway [3] Department of Urology, Oslo University Hospitals, Oslo, Norway.
University of Oslo · NOUniversity Medical Center Hamburg-Eppendorf · DEOslo University Hospital · NOUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is the second most common cause of cancer-associated deaths in men, and signaling via a transcription factor called androgen receptor (AR) is an important driver of the disease. Consequently, AR target genes are prominent candidates to be specific for prostate cancer and also important for the survival of the cancer cells. Here we assess the levels of all hexosamine biosynthetic pathway (HBP) enzymes in 15 separate clinical gene expression data sets and identify the last enzyme in the pathway, UDP-N-acetylglucosamine pyrophosphorylase 1 (UAP1), to be highly overexpressed in prostate cancer. We analyzed 3261 prostate cancers on a tissue microarray and found that UAP1 staining correlates negatively with Gleason score (P=0.0039) and positively with high AR expression (P<0.0001). Cells with high UAP1 expression have 10-fold increased levels of the HBP end-product, UDP-N-acetylglucosamine (UDP-GlcNAc). UDP-GlcNAc is essential for N-linked glycosylation occurring in the endoplasmic reticulum (ER) and high UAP1 expression associates with resistance against inhibitors of N-linked glycosylation (tunicamycin and 2-deoxyglucose) but not with a general ER stress-inducing agent, the calcium ionophore A23187. Knockdown of UAP1 expression re-sensitized cells towards inhibitors of N-linked glycosylation, as measured by proliferation and activation of ER stress markers. Taken together, we have identified an enzyme, UAP1, which is highly overexpressed in prostate cancer and protects cancer cells from ER stress conferring a growth advantage.

Indexed as

Cell Line, TumorCell ProliferationDeoxyglucoseEndoplasmic ReticulumGalactosyltransferasesGlycosylationHumansMaleProstatic NeoplasmsReceptors, AndrogenTissue Array AnalysisTunicamycinUp-RegulationAR protein, humanDeoxyglucoseGalactosyltransferasesReceptors, AndrogenTunicamycinUDP-GalNAc pyrophosphorylase AGX1, human

Identifiers

PMID25241896
OpenAlexW2006022605

What OpenQuestion holds

Textmetadata
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.