{"title":"miR-574-3p调节Smad/Snail信号通路促进鼻咽癌细胞上皮-间质转化","authors":"Ping Ai, Wei Qu, Xianbing Peng, Yi Zeng","doi":"10.1007/s10528-025-11182-4","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":1.6000,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"miR-574-3p Regulates Smad/Snail Signaling to Promote Epithelial-Mesenchymal Transition in Nasopharyngeal Carcinoma Cells.\",\"authors\":\"Ping Ai, Wei Qu, Xianbing Peng, Yi Zeng\",\"doi\":\"10.1007/s10528-025-11182-4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":482,\"journal\":{\"name\":\"Biochemical Genetics\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2025-07-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochemical Genetics\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1007/s10528-025-11182-4\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemical Genetics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s10528-025-11182-4","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
miR-574-3p Regulates Smad/Snail Signaling to Promote Epithelial-Mesenchymal Transition in Nasopharyngeal Carcinoma Cells.
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.
期刊介绍:
Biochemical Genetics welcomes original manuscripts that address and test clear scientific hypotheses, are directed to a broad scientific audience, and clearly contribute to the advancement of the field through the use of sound sampling or experimental design, reliable analytical methodologies and robust statistical analyses.
Although studies focusing on particular regions and target organisms are welcome, it is not the journal’s goal to publish essentially descriptive studies that provide results with narrow applicability, or are based on very small samples or pseudoreplication.
Rather, Biochemical Genetics welcomes review articles that go beyond summarizing previous publications and create added value through the systematic analysis and critique of the current state of knowledge or by conducting meta-analyses.
Methodological articles are also within the scope of Biological Genetics, particularly when new laboratory techniques or computational approaches are fully described and thoroughly compared with the existing benchmark methods.
Biochemical Genetics welcomes articles on the following topics: Genomics; Proteomics; Population genetics; Phylogenetics; Metagenomics; Microbial genetics; Genetics and evolution of wild and cultivated plants; Animal genetics and evolution; Human genetics and evolution; Genetic disorders; Genetic markers of diseases; Gene technology and therapy; Experimental and analytical methods; Statistical and computational methods.