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<p>Progress in molecular medicine has resulted in novel cancer therapies, with microRNAs (miRNAs) recognized as promising instruments for cancer detection and treatment. MicroRNAs are tiny non-coding RNA sequences that manipulate gene expression at the post-transcriptional stage and are involved in cellular differentiation and death. miR-32-5p demonstrates oncogenic activity in several cancers, while c-MYC oncogene is a well-known driver of cancer, promoting tumor growth by stimulating cell proliferation, blocking apoptosis, and suppressing immune responses. This study aimed to examine how inhibiting miR-32-5p affected the behavior of breast tumor cells (MCF-7), particularly focusing on changes in cellular apoptosis and proliferation, and to investigate its relationship with c-MYC expression. A locked nucleic acid (LNA)-based inhibitor was used to knock down miR-32-5p in MCF-7 breast cancer cells. Cell viability was assessed using MTT assays at 24, 48, and 72 h post-transfection. Apoptotic and necrotic cell populations were differentiated using Annexin-V labeling with Propidium iodide. Expression levels of miR-32-5p and c-MYC were evaluated using quantitative Real-Time PCR before and after transfection with the miR-32-5p inhibitor. Inhibition of miR-32-5p significantly reduced MCF-7 cell viability at 48 h post-transfection (<i>P</i> &lt; 0.002) and increased apoptotic cells to approximately 17% (vs. 0.3% in controls, <i>P</i> &lt; 0.05), concomitant with significant downregulation of c-MYC mRNA (<i>P</i> &lt; 0.006). The lowest level of miR-32-5p expression was observed at 48 h following transfection, with levels gradually increasing by 72 h. This study is the first to demonstrate a plausible regulatory relationship between miR-32-5p and c-MYC in breast tumor cells. The significant reduction in cell viability and increase in apoptosis following miR-32-5p inhibition, likely mediated through c-MYC downregulation, suggests a plausible pathway that may be targeted for therapeutic intervention in breast cancer.</p> Graphical abstract <p></p>

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Targeting miR-32-5p suppresses c-MYC-driven proliferation and induces apoptosis in MCF-7 breast cancer cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月25日

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  • Ahmed I. Khoder,
  • I. H. El-Sayed,
  • Yasser B. M. Ali

摘要

Progress in molecular medicine has resulted in novel cancer therapies, with microRNAs (miRNAs) recognized as promising instruments for cancer detection and treatment. MicroRNAs are tiny non-coding RNA sequences that manipulate gene expression at the post-transcriptional stage and are involved in cellular differentiation and death. miR-32-5p demonstrates oncogenic activity in several cancers, while c-MYC oncogene is a well-known driver of cancer, promoting tumor growth by stimulating cell proliferation, blocking apoptosis, and suppressing immune responses. This study aimed to examine how inhibiting miR-32-5p affected the behavior of breast tumor cells (MCF-7), particularly focusing on changes in cellular apoptosis and proliferation, and to investigate its relationship with c-MYC expression. A locked nucleic acid (LNA)-based inhibitor was used to knock down miR-32-5p in MCF-7 breast cancer cells. Cell viability was assessed using MTT assays at 24, 48, and 72 h post-transfection. Apoptotic and necrotic cell populations were differentiated using Annexin-V labeling with Propidium iodide. Expression levels of miR-32-5p and c-MYC were evaluated using quantitative Real-Time PCR before and after transfection with the miR-32-5p inhibitor. Inhibition of miR-32-5p significantly reduced MCF-7 cell viability at 48 h post-transfection (P < 0.002) and increased apoptotic cells to approximately 17% (vs. 0.3% in controls, P < 0.05), concomitant with significant downregulation of c-MYC mRNA (P < 0.006). The lowest level of miR-32-5p expression was observed at 48 h following transfection, with levels gradually increasing by 72 h. This study is the first to demonstrate a plausible regulatory relationship between miR-32-5p and c-MYC in breast tumor cells. The significant reduction in cell viability and increase in apoptosis following miR-32-5p inhibition, likely mediated through c-MYC downregulation, suggests a plausible pathway that may be targeted for therapeutic intervention in breast cancer.

Graphical abstract