ArticleGenes & genomics2026
MicroRNA-124 induces AML differentiation and apoptosis through c-Myc suppression.
Article in Genes & genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
Abstract
backgroundAcute myeloid leukemia (AML) is a hematologic malignancy marked by blocked differentiation and uncontrolled proliferation. While miR-124 has been implicated as a tumor suppressor in various cancers, its functional role in AML remains unclear.
objectiveThis study aimed to investigate the anti-leukemic effects of miR-124 and its regulatory mechanisms involving c-Myc and ROS signaling in AML.
methodsAML cells were engineered to overexpress miR-124. Functional assays including flow cytometry, viability, and apoptosis analyses were conducted. ROS levels were measured, and c-Myc regulation was evaluated via western blotting, qPCR, ChIP, and pharmacological inhibition. Exosome-mediated delivery was also examined.
resultsmiR-124 overexpression induced AML cell differentiation and apoptosis, accompanied by ROS accumulation and c-Myc downregulation. ROS induction suppressed c-Myc and activated the p21/p16/Rb axis, promoting cell cycle arrest. ChIP assays revealed that c-Myc binds the miR-124 promoter, indicating a negative feedback loop. Combination treatment with miR-124 and a c-Myc inhibitor enhanced anti-proliferative effects. Additionally, miR-124-containing exosomes reduced AML cell viability.
conclusionsmiR-124 acts as a tumor suppressor in AML by modulating a ROS-dependent c-Myc signaling pathway and inducing differentiation and apoptosis. These findings highlight miR-124 as a promising therapeutic and prognostic target in AML.
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