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<p>This study investigates the tumor-suppressive role of miR-139-5p in hepatocellular carcinoma (HCC) and its molecular mechanism of regulating the AKT-mTOR signaling pathway through targeting spermidine oxidase (SMOX). Analysis of TCGA and UALCAN databases revealed significantly lower expression of miR-139-5p in HCC tissues and cell lines, which correlated with poor clinical prognosis. Further experiments demonstrated that miR-139-5p overexpression notably inhibited HCC cell proliferation, migration, and invasion. Additionally, dual-luciferase assays confirmed that SMOX is a target of miR-139-5p. SMOX was found to be overexpressed in HCC tissues and closely associated with adverse prognosis. The study also revealed that SMOX promotes HCC progression by activating the AKT-mTOR signaling pathway and epithelial-mesenchymal transition (EMT). Overexpression of SMOX significantly increased the phosphorylation levels of AKT, mTOR, and their downstream effectors, while upregulating EMT markers such as N-cadherin, vimentin, and Snail, and downregulating the epithelial marker E-cadherin. Rescue experiments demonstrated that miR-139-5p suppressed SMOX expression, thereby inhibiting the activation of the AKT-mTOR pathway and EMT, ultimately reducing HCC cell proliferation and invasion. This study, for the first time, elucidates the mechanism by which miR-139-5p suppresses HCC progression through targeting SMOX to inhibit the AKT-mTOR pathway and EMT. These findings suggest that both miR-139-5p and SMOX could serve as potential therapeutic targets for HCC treatment.</p>

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miR-139-5p suppresses hepatocellular carcinoma progression by targeting SMOX to inhibit AKT-mTOR pathway and epithelial-mesenchymal transition

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月24日

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  • Wenjun Pei,
  • Kai Li,
  • Yaping Bai,
  • Li Ren,
  • Anqi Mo,
  • Jianping Mei,
  • Hao Ding,
  • Ruiyang Wang,
  • Qianqian Zhao,
  • Hui Wang

摘要

This study investigates the tumor-suppressive role of miR-139-5p in hepatocellular carcinoma (HCC) and its molecular mechanism of regulating the AKT-mTOR signaling pathway through targeting spermidine oxidase (SMOX). Analysis of TCGA and UALCAN databases revealed significantly lower expression of miR-139-5p in HCC tissues and cell lines, which correlated with poor clinical prognosis. Further experiments demonstrated that miR-139-5p overexpression notably inhibited HCC cell proliferation, migration, and invasion. Additionally, dual-luciferase assays confirmed that SMOX is a target of miR-139-5p. SMOX was found to be overexpressed in HCC tissues and closely associated with adverse prognosis. The study also revealed that SMOX promotes HCC progression by activating the AKT-mTOR signaling pathway and epithelial-mesenchymal transition (EMT). Overexpression of SMOX significantly increased the phosphorylation levels of AKT, mTOR, and their downstream effectors, while upregulating EMT markers such as N-cadherin, vimentin, and Snail, and downregulating the epithelial marker E-cadherin. Rescue experiments demonstrated that miR-139-5p suppressed SMOX expression, thereby inhibiting the activation of the AKT-mTOR pathway and EMT, ultimately reducing HCC cell proliferation and invasion. This study, for the first time, elucidates the mechanism by which miR-139-5p suppresses HCC progression through targeting SMOX to inhibit the AKT-mTOR pathway and EMT. These findings suggest that both miR-139-5p and SMOX could serve as potential therapeutic targets for HCC treatment.