Evidence map›Paper›PMID 39355364›Full record

ArticleNagoya journal of medical science2024

Crucial roles of exosomes secreted from ganglioside GD3/GD2-positive glioma cells in enhancement of the malignant phenotypes and signals of GD3/GD2-negative glioma cells.

Mohammad Abul Hasnat, Yuhsuke Ohmi, Farhana Yesmin, Mariko Kambe, Yoshiyuki Kawamoto, Robiul H Bhuiyan, Momoka Mizutani, Noboru Hashimoto, Akiko Tsuchida, Yuki Ohkawa and 4 more

Abstract read
In one paragraph

Article in Nagoya journal of medical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Flow Cytometry Analysis of Gangliosides Expressed on Extracellular Vesicles.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  2. Review
  3. Review
  4. 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

14 authors.

Mohammad Abul HasnatDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Yuhsuke OhmiDepartment of Clinical Engineering, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Farhana YesminDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Mariko KambeDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Yoshiyuki KawamotoDepartment of Immunology, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Robiul H BhuiyanDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Momoka MizutaniDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Noboru HashimotoDepartment of Tissue Regeneration, Tokushima University School of Dentistry, Tokushima, Japan.
Akiko TsuchidaLaboratory of Glyco-bioengineering, The Noguchi Institute, Tokyo, Japan.
Yuki OhkawaOsaka International Cancer Institute, Osaka, Japan.
Kei KanekoDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Orie TajimaDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Keiko FurukawaDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.
Koichi FurukawaDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroectoderm-derived tumors characteristically express gangliosides such as GD3 and GD2. Many studies have reported that gangliosides GD3/GD2 enhance malignant phenotypes of cancers. Recently, we reported that human gliomas expressing GD3/GD2 exhibited enhanced malignant phenotypes. Here, we investigated the function of GD3/GD2 in glioma cells and GD3/GD2-expressing glioma-derived exosomes. As reported previously, transfectant cells of human glioma U251 MG expressing GD3/GD2 showed enhanced cancer phenotypes compared with GD3/GD2-negative controls. When GD3/GD2-negative cells were treated with exosomes secreted from GD3/GD2-positive cells, clearly increased malignant properties were observed. Furthermore, increased phosphorylation of signaling molecules was detected after 5-15 min of exosome treatment, ie, higher tyrosine phosphorylation of platelet-derived growth factor receptor, focal adhesion kinase, and paxillin was found in treated cells than in controls. Phosphorylation of extracellular signal-regulated kinase-1/2 was also enhanced. Consequently, it is suggested that exosomes secreted from GD3/GD2-positive gliomas play important roles in enhancement of the malignant properties of glioma cells, leading to total aggravation of heterogenous cancer tissues, and also in the regulation of tumor microenvironments.

Indexed as

ExosomesGangliosidesGliomaPhenotypeBrain NeoplasmsCell Line, TumorHumansPaxillinPhosphorylationSignal Transductionganglioside, GD2ganglioside, GD3GangliosidesPaxillinexosomegangliosidegliomamalignancy

Identifiers

PMID39355364
PMCPMC11439612

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Registered trials

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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.