Evidence map›Paper›PMID 21949119›Full record

ArticleThe Journal of biological chemistry2011

A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.

Alessandro Prinetti, Ting Cao, Giuditta Illuzzi, Simona Prioni, Massimo Aureli, Nicoletta Gagliano, Giovanni Tredici, Virginia Rodriguez-Menendez, Vanna Chigorno, Sandro Sonnino

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of Sphingolipids in Cancer Immunotherapy.International journal of molecular sciences · 2021
    Review
  4. Article
  5. Different Role of Caveolin-1 Gene in the Progression of Gynecological Tumors.Asian Pacific journal of cancer prevention : APJCP · 2019
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. GM3 and cancer.Glycoconjugate journal · 2015
    Review
  13. Lesser-Known Molecules in Ovarian Carcinogenesis.BioMed research international · 2015
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Glycosphingolipid Mediated Caveolin-1 Oligomerization.Journal of glycomics & lipidomics · 2012
    Article
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 2 institutions in 1 country.

Alessandro PrinettiDepartment of Medical Chemistry, Biochemistry and Biotechnology, University of Milan, 20090 Segrate, Italy. alessandro.prinetti@unimi.it
Ting Cao
Giuditta Illuzzi
Simona Prioni
Massimo Aureli
Nicoletta Gagliano
Giovanni Tredici
Virginia Rodriguez-Menendez
Vanna Chigorno
Sandro Sonnino
University of Milan · ITUniversity of Milano-Bicocca · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma.

Indexed as

Cell MovementSignal TransductionCaveolin 1Cell Line, TumorCSK Tyrosine-Protein KinaseEnzyme ActivationEnzyme InhibitorsFemaleGangliosidesGene SilencingGlucosyltransferasesHumansIntegrinsOvarian NeoplasmsProtein SubunitsProtein-Tyrosine KinasesCaveolin 1ceramide glucosyltransferaseCSK protein, humanCSK Tyrosine-Protein KinaseEnzyme InhibitorsGangliosidesGlucosyltransferaseshaematoside synthetaseIntegrinsProtein SubunitsProtein-Tyrosine KinasesSialyltransferasessrc-Family Kinases

Identifiers

PMID21949119
PMCPMC3220459
OpenAlexW2142754187

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.