Evidence map›Paper›PMID 34145699›Full record

ArticleCancer science2021

Lack of GD3 synthase (St8sia1) attenuates malignant properties of gliomas in genetically engineered mouse model.

Yuki Ohkawa, Pu Zhang, Hiroyuki Momota, Akira Kato, Noboru Hashimoto, Yuhsuke Ohmi, Robiul H Bhuiyan, Yesmin Farhana, Atsushi Natsume, Toshihiko Wakabayashi and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  8. Advances in Mass Spectrometry of Gangliosides Expressed in Brain Cancers.International journal of molecular sciences · 2024
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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

12 authors at 3 institutions in 1 country.

Yuki OhkawaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Pu ZhangDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Hiroyuki MomotaDepartment of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Akira KatoDepartment of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Noboru HashimotoDepartment of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yuhsuke OhmiDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Robiul H BhuiyanDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Yesmin FarhanaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Atsushi NatsumeDepartment of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID https://orcid.org/0000-0002-9113-0470
Toshihiko WakabayashiDepartment of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Keiko FurukawaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Koichi FurukawaDepartment of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.ORCID https://orcid.org/0000-0002-3321-9784
Chubu University · JPNagoya University · JPTokyo Medical University · JP

Funding

Ministry of Education, Culture, Sports and Technology of Japan (MEXT) and JST-CREST 15H04696Ministry of Education, Culture, Sports and Technology of Japan (MEXT) and JST-CREST 23110008Ministry of Education, Culture, Sports and Technology of Japan (MEXT) and JST-CREST 24390078Ministry of Education, Culture, Sports and Technology of Japan (MEXT) and JST-CREST 25670141Ministry of Education, Culture, Sports and Technology of Japan (MEXT) and JST-CREST JPMJCR17H2
6 · The paper itself

Abstract

High expression of gangliosides GD3 and GD2 is observed in human gliomas. The functions of GD3 and GD2 in malignant properties have been reported in glioma cells in vitro, but those functions have not yet been investigated in vivo. In this study, we showed that deficiency of GD3 synthase (GD3S, St8sia1) attenuated glioma progression and clinical and pathological features in a platelet-derived growth factor B-driven murine glioma model. Lack of GD3S resulted in the prolonged lifespan of glioma-bearing mice and low-grade pathology in generated gliomas. Correspondingly, they showed reduced phosphorylation levels of Akt, Erks, and Src family kinases in glioma tissues. A DNA microarray study revealed marked alteration in the expression of various genes, particularly in MMP family genes, in GD3S-deficient gliomas. Re-expression of GD3S restored expression of MMP9 in primary-cultured glioma cells. We also identified a transcription factor, Ap2α, expressed in parallel with GD3S expression, and showed that Ap2α was critical for the induction of MMP9 by transfection of its cDNA and luciferase reporter genes, and a ChIP assay. These findings suggest that GD3S enhances the progression of gliomas by enhancement of the Ap2α-MMP9 axis. This is the first report to describe the tumor-enhancing functions of GD3S in vivo.

Indexed as

Disease Models, AnimalAnimalsAstrocytesBrain NeoplasmsCells, CulturedDisease ProgressionGangliosidesGene Expression Regulation, NeoplasticGliomaLongevityMatrix Metalloproteinase 9MiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutSialyltransferasesalpha-N-acetylneuraminate alpha-2,8-sialyltransferaseganglioside, GD2ganglioside, GD3GangliosidesMatrix Metalloproteinase 9Mmp9 protein, mouseSialyltransferasesgangliosidegliomaknockoutmatrix metalloproteinasesialyltransferase

Identifiers

PMID34145699
PMCPMC8409297
OpenAlexW3170588509

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.