Evidence map›Paper›PMID 35896929›Full record

ReviewCellular and molecular neurobiology2023

Genes of the Ubiquitin Proteasome System Qualify as Differential Markers in Malignant Glioma of Astrocytic and Oligodendroglial Origin.

Jerry Vriend, Thomas Klonisch

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Role of UBE2C in Brain Cancer Invasion and Dissemination.International journal of molecular sciences · 2023
    Review
  9. Review
  10. 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

2 authors at 1 institution in 1 country.

Jerry VriendDepartment of Human Anatomy and Cell Science, Max Rady College of Medicine, Max Rady Faculty of Health Sciences, University of Manitoba, Rm34, BMSB, 745 Bannatyne Ave, Winnipeg, MB, R3E0J9, Canada. Jerry.Vriend@umanitoba.ca.ORCID http://orcid.org/0000-0001-6435-755X
Thomas KlonischDepartment of Human Anatomy and Cell Science, Max Rady College of Medicine, Max Rady Faculty of Health Sciences, University of Manitoba, Rm34, BMSB, 745 Bannatyne Ave, Winnipeg, MB, R3E0J9, Canada.ORCID http://orcid.org/0000-0003-0448-6741
University of Manitoba · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have mined public genomic datasets to identify genes coding for components of the ubiquitin proteasome system (UPS) that may qualify as potential diagnostic and therapeutic targets in the three major glioma types, astrocytoma (AS), glioblastoma (GBM), and oligodendroglioma (ODG). In the Sun dataset of glioma (GEO ID: GSE4290), expression of the genes UBE2S and UBE2C, which encode ubiquitin conjugases important for cell-cycle progression, distinguished GBM from AS and ODG. KEGG analysis showed that among the ubiquitin E3 ligase genes differentially expressed, the Notch pathway was significantly over-represented, whereas among the E3 ligase adaptor genes the Hippo pathway was over-represented. We provide evidence that the UPS gene contributions to the Notch and Hippo pathway signatures are related to stem cell pathways and can distinguish GBM from AS and ODG. In the Sun dataset, AURKA and TPX2, two cell-cycle genes coding for E3 ligases, and the cell-cycle gene coding for the E3 adaptor CDC20 were upregulated in GBM. E3 ligase adaptor genes differentially expressed were also over-represented for the Hippo pathway and were able to distinguish classic, mesenchymal, and proneural subtypes of GBM. Also over-expressed in GBM were PSMB8 and PSMB9, genes encoding subunits of the immunoproteasome. Our transcriptome analysis provides a strong rationale for UPS members as attractive therapeutic targets for the development of more effective treatment strategies in malignant glioma. Ubiquitin proteasome system and glioblastoma: E1-ubiquitin-activating enzyme, E2-ubiquitin-conjugating enzyme, E3-ubiquitin ligase. Ubiquitinated substrates of E3 ligases may be degraded by the proteasome. Expression of genes for specific E2 conjugases, E3 ligases, and genes for proteasome subunits may serve as differential markers of subtypes of glioblastoma.

Indexed as

GlioblastomaGliomaHumansProteasome Endopeptidase ComplexUbiquitinUbiquitin-Conjugating EnzymesUbiquitin-Protein LigasesProteasome Endopeptidase ComplexUbe2S protein, humanUbiquitinUbiquitin-Conjugating EnzymesUbiquitin-Protein LigasesCDC20GlioblastomaImmunoproteasomeUbiquitin conjugaseUbiquitin ligase

Identifiers

PMID35896929
PMCPMC10079750
OpenAlexW4288068679

What Socratic 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 Socratic graph.