Possible regulation of ganglioside GD3 synthase gene expression with DNA methylation in human glioma cells.


Journal

Glycoconjugate journal
ISSN: 1573-4986
Titre abrégé: Glycoconj J
Pays: United States
ID NLM: 8603310

Informations de publication

Date de publication:
06 2023
Historique:
received: 30 11 2022
accepted: 21 02 2023
revised: 02 02 2023
medline: 24 5 2023
pubmed: 11 3 2023
entrez: 10 3 2023
Statut: ppublish

Résumé

Gangliosides are expressed in nervous systems and some neuroectoderm-derived tumors at high levels and play pivotal roles. However, mechanisms for the regulation of glycosyltransferase genes responsible for the ganglioside synthesis are not well understood. In this study, we analyzed DNA methylation patterns of promoter regions of GD3 synthase (ST8SIA1) as well as mRNA levels and ganglioside expression using human glioma cell lines. Among 5 cell lines examined, 4 lines showed changes in the expression levels of related genes after treatment with 5-aza-dC. LN319 showed up-regulation of St8sia1 and increased b-series gangliosides after 5-aza-dC treatment, and an astrocytoma cell line, AS showed high expression of ST8SIA1 and b-series gangliosides persistently before and after 5-Aza-2'-deoxycytidine treatment. Using these 2 cell lines, DNA methylation patterns of the promoter regions of the gene were analyzed by bisulfite-sequencing. Consequently, 2 regions that were methylated before 5-Aza-2'-deoxycytidine treatment were demethylated in LN319 after the treatment, while those regions were persistently demethylated in AS. These 2 regions corresponded with sites defined as promoter regions by Luciferase assay. Taken together, it was suggested that ST8SIA1 gene is regulated by DNA methylation at the promoter regions, leading to the regulation of tumor phenotypes.

Identifiants

pubmed: 36897478
doi: 10.1007/s10719-023-10108-9
pii: 10.1007/s10719-023-10108-9
doi:

Substances chimiques

Azacitidine M801H13NRU
Decitabine 776B62CQ27
ganglioside, GD3 62010-37-1
Gangliosides 0
alpha-N-acetylneuraminate alpha-2,8-sialyltransferase EC 2.4.99.8

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

323-332

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Yurie Yamamoto (Y)

Department of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Ken Higashimoto (K)

Department of Biomolecular Sciences, Division of Molecular Genetics & Epigenetics, Saga University Faculty of Medicine, Saga, Japan.

Yuki Ohkawa (Y)

Department of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Hidenobu Soejima (H)

Department of Biomolecular Sciences, Division of Molecular Genetics & Epigenetics, Saga University Faculty of Medicine, Saga, Japan.

Kei Kaneko (K)

Department of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.

Yuhsuke Ohmi (Y)

Department of Clinical Engineering, Chubu University College of Life and Health Sciences, Kasugai, Japan.

Keiko Furukawa (K)

Department of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.

Koichi Furukawa (K)

Department of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya, Japan. koichi@isc.chubu.ac.jp.
Department of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan. koichi@isc.chubu.ac.jp.

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