*Result*: Discovery of the selective chemical probe for protein methyltransferase METTL13 by biological evaluation and molecular dynamics simulation.

Title:
Discovery of the selective chemical probe for protein methyltransferase METTL13 by biological evaluation and molecular dynamics simulation.
Authors:
Zhang M; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Yu Q; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Zhang B; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China., Zhu H; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Sun J; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, State Key laboratory of Experimental Hematology, Department of Chemical Biology, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Xiao S; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Yan K; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Yan D; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Qin Y; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Xi C; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Wang L; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, State Key laboratory of Experimental Hematology, Department of Chemical Biology, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China., Dong C; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China. Electronic address: dongcheng@tmu.edu.cn., Ma Y; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China. Electronic address: maying@tmu.edu.cn., Chen D; Department of Medicinal Chemistry, Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China. Electronic address: chendongxing@tmu.edu.cn.
Source:
Bioorganic chemistry [Bioorg Chem] 2026 Feb; Vol. 169, pp. 109426. Date of Electronic Publication: 2025 Dec 23.
Publication Type:
Journal Article
Language:
English
Journal Info:
Publisher: Elsevier Country of Publication: United States NLM ID: 1303703 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2120 (Electronic) Linking ISSN: 00452068 NLM ISO Abbreviation: Bioorg Chem Subsets: MEDLINE
Imprint Name(s):
Publication: Amsterdam : Elsevier
Original Publication: New York, London, Academic Press.
Contributed Indexing:
Keywords: Bisubstrate analogs; Chemical probe; MD simulation; METTL13
Substance Nomenclature:
EC 2.1.1.- (Methyltransferases)
0 (Enzyme Inhibitors)
Entry Date(s):
Date Created: 20251230 Date Completed: 20260119 Latest Revision: 20260119
Update Code:
20260130
DOI:
10.1016/j.bioorg.2025.109426
PMID:
41468753
Database:
MEDLINE

*Further Information*

*METTL13, a dual-functional methyltransferase harboring protein N-terminal methyltransferase (NTMT) activity, has emerged as a pivotal regulator in carcinogenesis, tumor progression, and patient prognosis, thereby garnering substantial interest as a promising therapeutic target for cancers. Despite its clinical significance, no specific chemical probes or inhibitors have been reported to date, highlighting an urgent need for drug discovery efforts targeting this enzyme. Herein, we employed the bisubstrate inhibitor strategy to develop the chemical probe NT32 for METTL13, which showed selective against a panel of methyltransferases. Comprehensive investigations into the structural and functional impacts of NT32 on METTL13 were conducted via molecular docking, molecular dynamics (MD) simulations, and multi-dimensional analyses. Computational modeling revealed that NT32 could occupy both the SAM/SAH-binding pocket and the peptide substrate-binding site of METTL13 simultaneously, establishing a bivalent binding mode. Notably, MD simulations unveiled significant enhancements in both positive and negative residue correlations within the NT32-METTL13 complex compared to the wild-type enzyme. Specifically, interactions between NT32 and critical residues (Gly503, Asn614, Gly644, Glu645) strengthened the connectivity of Met692 with its surrounding residues. This structural reorganization was accompanied by augmented correlated motions between the Gly501-Val511 region (loop<subscript>501-504</subscript>-α2<subscript>505-511</subscript>) and the Leu613-Leu620 segment (β5<subscript>613-615</subscript>-loop<subscript>616-618</subscript>-α6<subscript>619-620</subscript>), culminating in a more compact and stable protein conformation. Furthermore, NT32 specifically targeted and stabilized METTL13 in cellular thermal shift assay. These findings not only provide mechanistic insights into NT32-METTL13 interactions but also pave the way for discovery of METTL13 probes or inhibitors.
(Copyright © 2025 Elsevier Inc. All rights reserved.)*

*Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dongxing Chen reports financial support was provided by National Natural Science Foundation of China. Dongxing Chen reports financial support was provided by Tianjin Municipal Science and Technology Bureau. Dongxing Chen reports financial support was provided by Tianjin Municipal Education Commission. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.*