Prediction of the binding mechanism of a selective DNA methyltransferase 3A inhibitor by molecular simulation.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
12 06 2024
Historique:
received: 08 12 2023
accepted: 06 06 2024
medline: 13 6 2024
pubmed: 13 6 2024
entrez: 12 6 2024
Statut: epublish

Résumé

DNA methylation is an epigenetic mechanism that introduces a methyl group at the C5 position of cytosine. This reaction is catalyzed by DNA methyltransferases (DNMTs) and is essential for the regulation of gene transcription. The DNMT1 and DNMT3A or -3B family proteins are known targets for the inhibition of DNA hypermethylation in cancer cells. A selective non-nucleoside DNMT3A inhibitor was developed that mimics S-adenosyl-l-methionine and deoxycytidine; however, the mechanism of selectivity is unclear because the inhibitor-protein complex structure determination is absent. Therefore, we performed docking and molecular dynamics simulations to predict the structure of the complex formed by the association between DNMT3A and the selective inhibitor. Our simulations, binding free energy decomposition analysis, structural isoform comparison, and residue scanning showed that Arg688 of DNMT3A is involved in the interaction with this inhibitor, as evidenced by its significant contribution to the binding free energy. The presence of Asn1192 at the corresponding residues in DNMT1 results in a loss of affinity for the inhibitor, suggesting that the interactions mediated by Arg688 in DNMT3A are essential for selectivity. Our findings can be applied in the design of DNMT-selective inhibitors and methylation-specific drug optimization procedures.

Identifiants

pubmed: 38866895
doi: 10.1038/s41598-024-64236-9
pii: 10.1038/s41598-024-64236-9
doi:

Substances chimiques

DNA (Cytosine-5-)-Methyltransferases EC 2.1.1.37
DNA Methyltransferase 3A EC 2.1.1.37
Enzyme Inhibitors 0
DNMT3A protein, human 0
DNA (Cytosine-5-)-Methyltransferase 1 EC 2.1.1.37
DNMT1 protein, human EC 2.1.1.37

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

13508

Subventions

Organisme : Japan Society for the Promotion of Science
ID : JP21K06094
Organisme : Japan Society for the Promotion of Science
ID : JP23K16987
Organisme : Japan Agency for Medical Research and Development
ID : JP22ama121029j0002
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : JPMXP1020230120

Informations de copyright

© 2024. The Author(s).

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Auteurs

Genki Kudo (G)

Physics Department, Graduate School of Pure and Applied Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8571, Japan.

Takumi Hirao (T)

Doctoral Program in Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8575, Japan.
Division of Biomedical Science, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.

Ryuhei Harada (R)

Center for Computational Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8577, Japan.

Takatsugu Hirokawa (T)

Division of Biomedical Science, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.
Transborder Medical Research Center, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.

Yasuteru Shigeta (Y)

Physics Department, Graduate School of Pure and Applied Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8571, Japan.
Center for Computational Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8577, Japan.

Ryunosuke Yoshino (R)

Division of Biomedical Science, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. yoshino.r.aa@md.tsukuba.ac.jp.
Transborder Medical Research Center, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. yoshino.r.aa@md.tsukuba.ac.jp.

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