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Background <p>Acute 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.</p> Objective <p>This study aimed to investigate the anti-leukemic effects of miR-124 and its regulatory mechanisms involving c-Myc and ROS signaling in AML.</p> Methods <p>AML 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.</p> Results <p>miR-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.</p> Conclusions <p>miR-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.</p>

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MicroRNA-124 induces AML differentiation and apoptosis through c-Myc suppression

  • 期刊论文

  • 发表日期：

    2025年11月26日

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  • Byeol-Eun Jeon,
  • Chan-Seong Kwon,
  • Ji-Eun Lee,
  • Su-Ji Lee,
  • Kwonwoo Song,
  • Yun Ju Lee,
  • Du Hyeong Lee,
  • Sang-Woo Kim

摘要

Background

Acute 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.

Objective

This study aimed to investigate the anti-leukemic effects of miR-124 and its regulatory mechanisms involving c-Myc and ROS signaling in AML.

Methods

AML 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.

Results

miR-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.

Conclusions

miR-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.