Evidence map›Paper›PMID 22632091›Full record

ArticleCancer science2012

Enhancement of malignant properties of human osteosarcoma cells with disialyl gangliosides GD2/GD3.

Hidenobu Shibuya, Kazunori Hamamura, Hiroshi Hotta, Yasuyuki Matsumoto, Yoshihiro Nishida, Hisashi Hattori, Keiko Furukawa, Minoru Ueda, Koichi Furukawa

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.4field-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

65 citing papers in PubMed, 105 citations in OpenAlex.

  1. Immunotherapeutic Strategies Targeting GD2-Expressing Malignancies.Advances in experimental medicine and biology · 2026
    Review
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  3. Article
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  7. Article
  8. Review
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  11. Promise and Challenges of T Cell Immunotherapy for Osteosarcoma.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

5 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

9 authors at 2 institutions in 1 country.

Hidenobu ShibuyaDepartment of Biochemistry II, Nagoya University Graduate School of Medicine, Japan.
Kazunori Hamamura
Hiroshi Hotta
Yasuyuki Matsumoto
Yoshihiro Nishida
Hisashi Hattori
Keiko Furukawa
Minoru Ueda
Koichi Furukawa
Nagoya University · JPChubu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression and implications of gangliosides in human osteosarcomas have not been systematically analyzed. In this study, we showed that gangliosides GD3 and GD2 are highly expressed in the majority of human osteosarcoma cell lines derived from oral cavity regions. Introduction of GD3 synthase cDNA into a GD3/GD2-negative (GD3/GD2-) human osteosarcoma subline resulted in the establishment of GD3/GD2+ transfectant cells. They showed increased cell migration and invasion activities in wound healing and Boyden chamber invasion assays, respectively, compared to the control cells. When treated with serum, GD3/GD2+ cells showed stronger tyrosine phosphorylation of p130Cas, focal adhesion kinase, and paxillin than GD3/GD2- cells. In particular, paxillin underwent much stronger phosphorylation, suggesting its role in cell motility. Furthermore, we tried to dissect the roles of GD3 and GD2 in the malignant properties of the transfectant cells by establishing single ganglioside-expressing cells, that is, either GD3 or GD2. Although GD3/GD2+ cells showed the most malignant properties, GD2+ cells showed almost equivalent levels to GD3/GD2+ cells in invasion and migration activities, and in the intensities of tyrosine phosphorylation of paxillin. Among Src family kinases, Lyn was expressed predominantly, and was involved in the invasion and motility of GD3- and/or GD2-expressing transfectants. Furthermore, it was elucidated by gene silencing that Lyn was located in a different pathway from that of FAK to eventually lead paxillin activation. These results suggested that GD2/GD3 are responsible for the enhancement of the malignant features of osteosarcomas, and might be candidate targets in molecular-targeted therapy.

Indexed as

Bone NeoplasmsCell Line, TumorCell MovementCell ProliferationCrk-Associated Substrate ProteinFocal Adhesion Kinase 1GangliosidesGene ExpressionGene SilencingHumansOsteosarcomaPaxillinPhosphorylationSialyltransferasesSignal Transductionsrc-Family Kinasesalpha-N-acetylneuraminate alpha-2,8-sialyltransferaseCrk-Associated Substrate ProteinFocal Adhesion Kinase 1ganglioside, GD2ganglioside, GD3Gangliosideslyn protein-tyrosine kinasePaxillinPTK2 protein, humanSialyltransferasessrc-Family KinasesTyrosine

Identifiers

PMID22632091
PMCPMC7659376
OpenAlexW2077871666

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.