Evidence map›Paper›PMID 22730328›Full record

ArticleThe Journal of biological chemistry2012

O-linked β-N-acetylglucosaminylation (O-GlcNAcylation) in primary and metastatic colorectal cancer clones and effect of N-acetyl-β-D-glucosaminidase silencing on cell phenotype and transcriptome.

Galit Yehezkel, Liz Cohen, Adi Kliger, Esther Manor, Isam Khalaila

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Inhibition ofeLife · 2024
    Article
  3. Review
  4. Inhibition ofbioRxiv : the preprint server for biology · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Nutrient regulation of signaling and transcription.The Journal of biological chemistry · 2019
    Review
  14. O-GlcNAcylation of GLI transcription factors in hyperglycemic conditions augments Hedgehog activity.Laboratory investigation; a journal of technical methods and pathology · 2019
    Article
  15. Article
  16. Molecules (Basel, Switzerland) · 2018
    Article
  17. O-GlcNAc in cancer: An Oncometabolism-fueled vicious cycle.Journal of bioenergetics and biomembranes · 2018
    Review
  18. O-GlcNAcylation: key regulator of glycolytic pathways.Journal of bioenergetics and biomembranes · 2018
    Review
  19. AugmentedJournal of clinical biochemistry and nutrition · 2018
    Article
  20. 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

5 authors at 1 institution in 1 country.

Galit YehezkelFaculty of Engineering Sciences, The Avram and Stella Goldstein-Goren Department of Biotechnology Engineering, Ben-Gurion University of the Negev, P. O. Box 653, Beer-Sheva 84105, Israel.
Liz Cohen
Adi Kliger
Esther Manor
Isam Khalaila
Ben-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation is a regulatory post-translational modification occurring on the serine or threonine residues of nucleocytoplasmic proteins. O-GlcNAcylation is dynamically regulated by O-GlcNAc transferase and O-GlcNAcase (OGA), which are responsible for O-GlcNAc addition and removal, respectively. Although O-GlcNAcylation was found to play a significant role in several pathologies such as type II diabetes and neurodegenerative diseases, the role of O-GlcNAcylation in the etiology and progression of cancer remains vague. Here, we followed O-GlcNAcylation and its catalytic machinery in metastatic clones of human colorectal cancer and the effect of OGA knockdown on cellular phenotype and on the transcriptome. The colorectal cancer SW620 metastatic clone exhibited increased O-GlcNAcylation and decreased OGA expression compared with its primary clone, SW480. O-GlcNAcylation elevation in SW620 cells, through RNA interference of OGA, resulted in phenotypic alterations that included acquisition of a fibroblast-like morphology, which coincides with epithelial metastatic progression and growth retardation. Microarray analysis revealed that OGA silencing altered the expression of about 1300 genes, mostly involved in cell movement and growth, and specifically affected metabolic pathways of lipids and carbohydrates. These findings support the involvement of O-GlcNAcylation in various aspects of tumor cell physiology and suggest that this modification may serve as a link between metabolic changes and cancer.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticAcetylglucosaminidaseAdenocarcinomaColonic NeoplasmsGene SilencingGlycosylationHumansNeoplasm MetastasisNeoplasm ProteinsTranscriptomeAcetylglucosaminidaseNeoplasm Proteins

Identifiers

PMID22730328
PMCPMC3436545
OpenAlexW2064347847

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.