Biao Wang, Nianjie Zhang, Lin Dai, Yuanwei Zhang, Shuo Yin, Xuefeng Yang
{"title":"壬基酚通过上调miR-151a-3p促进结直肠癌细胞上皮-间质转化。","authors":"Biao Wang, Nianjie Zhang, Lin Dai, Yuanwei Zhang, Shuo Yin, Xuefeng Yang","doi":"10.1007/s12672-025-01805-y","DOIUrl":null,"url":null,"abstract":"<p><p>Nonylphenol (NP) is a common environmental contaminant and endocrine disruptor. Our previous research demonstrated that NP could promote the proliferation and epithelial-mesenchymal transition (EMT) of colorectal cancer (CRC) cells; however, the specific mechanism remains unclear. miRNA sequencing revealed that NP upregulated the expression levels of microRNA(miR)-151a-3p in CRC. Analysis of The Cancer Genome Atlas (TCGA) data revealed increased expression levels of miR-151a-3p in CRC tissues. The present experiments showed that NP could activate the WNT/β-catenin signaling pathway, and promoted the migration and invasion of CRC cells by increasing the expression levels of miR-151a-3p. Through bioinformatics analysis and dual-luciferase reporter assays, Fyn-related kinase (FRK) was identified as a target gene of miR-151a-3p. Knockdown of FRK promoted NP-induced EMT in CRC cells and activated the WNT/β-catenin signaling pathway, while overexpression had the opposite effect. In summary, the present study demonstrated that NP could inhibit FRK expression via miR-151a-3p, activate the WNT/β-catenin signaling pathway, and promote EMT in CRC cells.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"63"},"PeriodicalIF":2.8000,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11747012/pdf/","citationCount":"0","resultStr":"{\"title\":\"Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p.\",\"authors\":\"Biao Wang, Nianjie Zhang, Lin Dai, Yuanwei Zhang, Shuo Yin, Xuefeng Yang\",\"doi\":\"10.1007/s12672-025-01805-y\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Nonylphenol (NP) is a common environmental contaminant and endocrine disruptor. Our previous research demonstrated that NP could promote the proliferation and epithelial-mesenchymal transition (EMT) of colorectal cancer (CRC) cells; however, the specific mechanism remains unclear. miRNA sequencing revealed that NP upregulated the expression levels of microRNA(miR)-151a-3p in CRC. Analysis of The Cancer Genome Atlas (TCGA) data revealed increased expression levels of miR-151a-3p in CRC tissues. The present experiments showed that NP could activate the WNT/β-catenin signaling pathway, and promoted the migration and invasion of CRC cells by increasing the expression levels of miR-151a-3p. Through bioinformatics analysis and dual-luciferase reporter assays, Fyn-related kinase (FRK) was identified as a target gene of miR-151a-3p. Knockdown of FRK promoted NP-induced EMT in CRC cells and activated the WNT/β-catenin signaling pathway, while overexpression had the opposite effect. In summary, the present study demonstrated that NP could inhibit FRK expression via miR-151a-3p, activate the WNT/β-catenin signaling pathway, and promote EMT in CRC cells.</p>\",\"PeriodicalId\":11148,\"journal\":{\"name\":\"Discover. Oncology\",\"volume\":\"16 1\",\"pages\":\"63\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-01-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11747012/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Discover. Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s12672-025-01805-y\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Discover. Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12672-025-01805-y","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p.
Nonylphenol (NP) is a common environmental contaminant and endocrine disruptor. Our previous research demonstrated that NP could promote the proliferation and epithelial-mesenchymal transition (EMT) of colorectal cancer (CRC) cells; however, the specific mechanism remains unclear. miRNA sequencing revealed that NP upregulated the expression levels of microRNA(miR)-151a-3p in CRC. Analysis of The Cancer Genome Atlas (TCGA) data revealed increased expression levels of miR-151a-3p in CRC tissues. The present experiments showed that NP could activate the WNT/β-catenin signaling pathway, and promoted the migration and invasion of CRC cells by increasing the expression levels of miR-151a-3p. Through bioinformatics analysis and dual-luciferase reporter assays, Fyn-related kinase (FRK) was identified as a target gene of miR-151a-3p. Knockdown of FRK promoted NP-induced EMT in CRC cells and activated the WNT/β-catenin signaling pathway, while overexpression had the opposite effect. In summary, the present study demonstrated that NP could inhibit FRK expression via miR-151a-3p, activate the WNT/β-catenin signaling pathway, and promote EMT in CRC cells.