ArticleCell biology and toxicology2026
Acute myeloid leukemia (AML)-derived bone mesenchymal stem cell exosomal METTL14 promotes AML cell growth and glycolysis by HOXA3/WNT7B axis.
Article in Cell biology and toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute myeloid leukemia (AML)-derived bone mesenchymal stem cell (MSC) exosomes have been confirmed to have a positive effect on AML progression. This study aim to reveal the underlying molecular mechanism by which AML-MSC-derived exosomes promotes AML progression. AML-MSC was isolated from the bone marrow aspirates of AML patients. After incubated with AML-MSC, AML cell functions were analyzed. The expression levels of methyltransferase-like 14 (METTL14), homeobox A3 (HOXA3), WNT family member 7B (WNT7B) and glycolysis-related markers were examined. Exosomes were isolated from AML-MSC and then the obtained exosomes were co-cultured with AML cells. AML-MSC co-culturing could enhance AML cell proliferation and glycolysis, while repress cell apoptosis. METTL14 was upregulated in exosomes from AML-MSC, which could be ingested by AML cells. METTL14 could enhance HOXA3 mRNA stability via promoting its m6A modification. Knockdown of exosomal METTL14 from AML-MSC inhibited AML cell growth and glycolysis, while were reversed by HOXA3. In addition, HOXA3 bound to WNT7B promoter to increase its transcription, and WNT7B overexpression also eliminated si-HOXA3-mediated inhibitory on AML cell growth and glycolysis. Animal study revealed that knockdown of exosomal METTL14 from AML-MSC reduced AML tumorigenesis by decreasing HOXA3 and WNT7B expression. AML-MSC-derived exosomal METTL14 facilitated AML cell growth and glycolysis by activating the HOXA3/WNT7B axis, providing a new mechanism for understanding AML-MSC-derived exosomes to promote AML progression.
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