ArticleMolecular biology reports2026
METTL3-dependent m⁶A maturation of miR-140-3p contributes to hippocampal neuronal apoptosis through the OTX2/Wnt/β-catenin axis under chronic stress.
Article in Molecular biology reports, 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
backgroundChronic stress contributes to hippocampal neuronal apoptosis and neural circuit dysfunction in major depressive disorder (MDD), but the epitranscriptomic mechanisms regulating stress-responsive microRNAs remain unclear. This study investigated whether methyltransferase-like 3 (METTL3)-mediated N6-methyladenosine (m6A) modification promotes miR-140-3p maturation and neuronal apoptosis through the OTX2/Wnt/β-catenin axis under chronic stress. METHODS AND
resultsA chronic unpredictable mild stress rat model and a corticosterone-induced primary hippocampal neuron injury model were established. Behavioral assays, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining, flow cytometry, western blotting, qRT-PCR, proteomic and transcriptomic analyses, methylated RNA immunoprecipitation (MeRIP), DiGeorge syndrome critical region gene 8 (DGCR8) RNA immunoprecipitation (RIP), and dual-luciferase reporter assays were performed. Serum miR-140-3p expression was also assessed in patients with MDD and healthy controls. miR-140-3p was upregulated in the hippocampus of stressed rats and in the serum of patients with MDD. Hippocampal miR-140-3p knockdown alleviated depressive-like behaviors and reduced neuronal apoptosis, whereas miR-140-3p inhibition protected primary hippocampal neurons from corticosterone-induced apoptosis. Mechanistically, chronic stress increased METTL3 expression and global m6A levels. METTL3 enhanced m6A modification of pri-miR-140-3p, promoted DGCR8-dependent processing, and increased mature miR-140-3p expression. miR-140-3p directly targeted OTX2 and modulated Wnt/β-catenin signaling, while OTX2 silencing attenuated the antiapoptotic effect of miR-140-3p inhibition.
conclusionsMETTL3-dependent m6A maturation of miR-140-3p may contribute to stress-induced hippocampal neuronal apoptosis through the OTX2/Wnt/β-catenin axis, providing potential molecular targets for further investigation in MDD.
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