Evidence map›Paper›PMID 35267607›Full record

ReviewCancers2022

Role of GD3 Synthase ST8Sia I in Cancers.

Angelina Kasprowicz, Groux-Degroote Sophie, Chann Lagadec, Philippe Delannoy

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. EDF1 accelerates ganglioside GD3 accumulation to boost CD52-mediated CD8Journal of experimental & clinical cancer research : CR · 2025
    Article
  9. Review
  10. Article
  11. Ganglioside GD2 Contributes to a Stem-Like Phenotype in Intrahepatic Cholangiocarcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Gangliosides as Siglec ligands.Glycoconjugate journal · 2023
    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

4 authors at 1 institution in 1 country.

Angelina KasprowiczUniversity of Lille, CNRS, UMR 8576-UGSF-Unité de Glycosylation Structurale et Fonctionnelle, F-59000 Lille, France.
Groux-Degroote SophieUniversity of Lille, CNRS, UMR 8576-UGSF-Unité de Glycosylation Structurale et Fonctionnelle, F-59000 Lille, France.
Chann LagadecUniversity of Lille, CNRS, Inserm, CHU Lille UMR9020-U1277-CANTHER Cancer Heterogeneity, Plasticity and Resistance to Therapies, F-59000 Lille, France.ORCID 0000-0002-5182-2069
Philippe DelannoyUniversity of Lille, CNRS, UMR 8576-UGSF-Unité de Glycosylation Structurale et Fonctionnelle, F-59000 Lille, France.ORCID 0000-0001-6467-7553
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GD3 synthase controls the biosynthesis of complex gangliosides, bearing two or more sialic acid residues. Disialylated gangliosides GD3 and GD2 are tumor-associated carbohydrate antigens (TACA) in neuro-ectoderm-derived cancers, and are directly involved in cell malignant properties, i.e., migration, invasion, stemness, and epithelial-mesenchymal transition. Since GD3 and GD2 levels are directly linked to GD3 synthase expression and activity, targeting GD3 synthase appears to be a promising strategy through which to interfere with ganglioside-associated malignant properties. We review here the current knowledge on GD3 synthase expression and regulation in cancers, and the consequences of complex ganglioside expression on cancer cell signaling and properties, highlighting the relationships between GD3 synthase expression and epithelial-mesenchymal transition and stemness. Different strategies were used to modulate GD3 synthase expression in cancer cells in vitro and in animal models, such as inhibitors or siRNA/lncRNA, which efficiently reduced cancer cell malignant properties and the proportion of GD2 positive cancer stem cells, which are associated with high metastatic properties, resistance to therapy, and cancer relapse. These data show the relevance of targeting GD3 synthase in association with conventional therapies, to decrease the number of cancer stem cells in tumors.

Indexed as

epithelial–mesenchymal transitiongangliosideGD3 synthasetranscriptional regulation

Identifiers

PMID35267607
PMCPMC8909605
OpenAlexW4214944476

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.