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

被引:0
作者
Ai, Ping [1 ]
Qu, Wei [1 ]
Peng, Xianbing [1 ]
Zeng, Yi [1 ]
机构
[1] Shiyan Renmin Hosp, Dept Otolaryngol, Shiyan 442000, Hubei, Peoples R China
关键词
miR-574-3p; Smad/Snail signaling pathway; Epithelial-mesenchymal transition; Nasopharyngeal carcinoma; OPEN-LABEL; CHEMOTHERAPY; MULTICENTER; PROGRESSION; RECURRENT;
D O I
10.1007/s10528-025-11182-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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 (alpha-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.
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页数:12
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