Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p

被引:0
|
作者
Wang, Biao [1 ]
Zhang, Nianjie [1 ]
Dai, Lin [1 ]
Zhang, Yuanwei [1 ]
Yin, Shuo [1 ]
Yang, Xuefeng [1 ]
机构
[1] Zunyi Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 2, Zunyi 563006, Peoples R China
基金
中国国家自然科学基金;
关键词
Nonylphenol; Colorectal cancer; microRNA-151a-3p; Fyn-related kinase; WNT/beta-catenin; Epithelial-mesenchymal transition; METASTASIS; EXPRESSION;
D O I
10.1007/s12672-025-01805-y
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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/beta-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/beta-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/beta-catenin signaling pathway, and promote EMT in CRC cells.
引用
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页数:16
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