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<p>Epithelial<b>–</b>mesenchymal transition (EMT) is pivotal in the progression and metastasis of nasopharyngeal carcinoma (NPC). MicroRNAs (miRNAs), particularly miR-574-3p, are emerging as critical regulators in these processes. This study examines the role of miR-574-3p in NPC and its relationship with the Smad/Snail signaling pathway. Expression levels of miR-574-3p were analyzed in six NPC tumor tissues and adjacent normal tissues using qRT-PCR. Functional assays, including overexpression and inhibition of miR-574-3p, were conducted in HNE1 cells. Dual-luciferase reporter assays validated the targeting relationship between miR-574-3p and Smad7. EMT-related molecular changes were evaluated by Western blotting and migration assays. miR-574-3p was significantly upregulated in NPC tumor tissues compared to adjacent normal tissues. Overexpression of miR-574-3p promotes proliferation and migration and inhibits apoptosis in HNE1 cells. Moreover, miR-574-3p upregulation inhibited Smad7 and Snail expression, reducing EMT markers (α-SMA and Twist1), while its inhibition had the opposite effects. Dual-luciferase assays confirmed that miR-574-3p directly targets Smad7. This study reveals that miR-574-3p inhibits the EMT process of NPC cells by regulating the Smad/Snail signaling pathway, providing a new potential therapeutic target for the treatment of NPC.</p>

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miR-574-3p Regulates Smad/Snail Signaling to Promote Epithelial–Mesenchymal Transition in Nasopharyngeal Carcinoma Cells

  • 期刊论文

  • 发表日期：

    2025年7月9日

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  • Ping Ai,
  • Wei Qu,
  • Xianbing Peng,
  • Yi Zeng

摘要

Epithelial–mesenchymal transition (EMT) is pivotal in the progression and metastasis of nasopharyngeal carcinoma (NPC). MicroRNAs (miRNAs), particularly miR-574-3p, are emerging as critical regulators in these processes. This study examines the role of miR-574-3p in NPC and its relationship with the Smad/Snail signaling pathway. Expression levels of miR-574-3p were analyzed in six NPC tumor tissues and adjacent normal tissues using qRT-PCR. Functional assays, including overexpression and inhibition of miR-574-3p, were conducted in HNE1 cells. Dual-luciferase reporter assays validated the targeting relationship between miR-574-3p and Smad7. EMT-related molecular changes were evaluated by Western blotting and migration assays. miR-574-3p was significantly upregulated in NPC tumor tissues compared to adjacent normal tissues. Overexpression of miR-574-3p promotes proliferation and migration and inhibits apoptosis in HNE1 cells. Moreover, miR-574-3p upregulation inhibited Smad7 and Snail expression, reducing EMT markers (α-SMA and Twist1), while its inhibition had the opposite effects. Dual-luciferase assays confirmed that miR-574-3p directly targets Smad7. This study reveals that miR-574-3p inhibits the EMT process of NPC cells by regulating the Smad/Snail signaling pathway, providing a new potential therapeutic target for the treatment of NPC.