ArticleTranslational cancer research2025
METTL11A serves as a novel therapeutic target for acute myeloid leukemia through regulation of the p38-MAPK pathway.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Decoding Protein-Methylating METTLs in Humans: Structural, Functional, and Disease Insights over the Past Decade.International journal of molecular sciences · 2026Review
- Prognostic significance of NTMT1 and its association with tumor progression in oral squamous cell carcinoma.Frontiers in oncology · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute myeloid leukemia (AML) represents a heterogeneous blood malignancy and is the most common and severe acute leukemia in adult. The METTL gene family is increasingly being recognized as involved in cancer progression. The aim of the study is to elaborate on the specific role of METTL11A in AML. Methods: In this research, cell viability, transwell assay, and scratch wound assay were utilized to assess cell proliferation and migration in AML cells. Western blot was used to determine the expression of proteins and the activation of signal pathway. Virtual screening was performed to obtain potential inhibitors of METTL11A. Results: Our findings indicated that METTL11A expression levels were strongly associated with AML patients' prognosis. Overexpressed METTL11A by constructing stable cell lines promoted proliferation and migration in AML cells. Conversely, knockdown of METTL11A inhibited cell viability and migration. Through gene sets enrichment analysis, we validated the inactivated p38-mitogen-activated protein kinase (MAPK) pathway under silenced METTL11A expression. In high throughput molecular docking, S-Adenosyl-L-methionine disulfate tosylate was predicted to bind METTL11A, which was validated to inhibit cell proliferation and migration. Conclusions: The results suggested that METTL11A is a novel biomarker and therapeutic target in AML, which is mediated by suppressed MAPK pathway.
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