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miR-574-3p通过调控Smad/Snail信号通路促进鼻咽癌细胞上皮-间质转化

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

作者信息

Ai Ping, Qu Wei, Peng Xianbing, Zeng Yi

机构信息

Department of Otolaryngology, Shiyan Renmin Hospital, Shiyan, 442000, Hubei, People's Republic of China.

出版信息

Biochem Genet. 2025 Jul 9. doi: 10.1007/s10528-025-11182-4.

Abstract

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.

摘要

上皮-间质转化(EMT)在鼻咽癌(NPC)的进展和转移中起关键作用。微小RNA(miRNA),尤其是miR-574-3p,正在成为这些过程中的关键调节因子。本研究探讨miR-574-3p在NPC中的作用及其与Smad/Snail信号通路的关系。使用qRT-PCR分析了6个NPC肿瘤组织和相邻正常组织中miR-574-3p的表达水平。在HNE1细胞中进行了包括miR-574-3p过表达和抑制在内的功能测定。双荧光素酶报告基因测定验证了miR-574-3p与Smad7之间的靶向关系。通过蛋白质印迹和迁移测定评估EMT相关的分子变化。与相邻正常组织相比,NPC肿瘤组织中miR-574-3p显著上调。miR-574-3p的过表达促进HNE1细胞的增殖和迁移并抑制其凋亡。此外,miR-574-3p的上调抑制了Smad7和Snail的表达,减少了EMT标志物(α-SMA和Twist1),而其抑制则产生相反的效果。双荧光素酶测定证实miR-574-3p直接靶向Smad7。本研究表明,miR-574-3p通过调节Smad/Snail信号通路抑制NPC细胞的EMT过程,为NPC的治疗提供了一个新的潜在治疗靶点。

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