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

Abstract 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 seq...

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Main Authors: Biao Wang, Nianjie Zhang, Lin Dai, Yuanwei Zhang, Shuo Yin, Xuefeng Yang
Format: Article
Language:English
Published: Springer 2025-01-01
Series:Discover Oncology
Subjects:
Online Access:https://doi.org/10.1007/s12672-025-01805-y
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author Biao Wang
Nianjie Zhang
Lin Dai
Yuanwei Zhang
Shuo Yin
Xuefeng Yang
author_facet Biao Wang
Nianjie Zhang
Lin Dai
Yuanwei Zhang
Shuo Yin
Xuefeng Yang
author_sort Biao Wang
collection DOAJ
description Abstract 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.
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institution Kabale University
issn 2730-6011
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publishDate 2025-01-01
publisher Springer
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series Discover Oncology
spelling doaj-art-7173e9176f4543a7a7b6f07319d8a1da2025-01-26T12:39:44ZengSpringerDiscover Oncology2730-60112025-01-0116111610.1007/s12672-025-01805-yNonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3pBiao Wang0Nianjie Zhang1Lin Dai2Yuanwei Zhang3Shuo Yin4Xuefeng Yang5Department of Gastrointestinal Surgery, The Second Affiliated Hospital of Zunyi Medical UniversityDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Zunyi Medical UniversityDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Zunyi Medical UniversityDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Zunyi Medical UniversityDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Zunyi Medical UniversityDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Zunyi Medical UniversityAbstract 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.https://doi.org/10.1007/s12672-025-01805-yNonylphenolColorectal cancermicroRNA-151a-3pFyn-related kinaseWNT/β-cateninEpithelial-mesenchymal transition
spellingShingle Biao Wang
Nianjie Zhang
Lin Dai
Yuanwei Zhang
Shuo Yin
Xuefeng Yang
Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p
Discover Oncology
Nonylphenol
Colorectal cancer
microRNA-151a-3p
Fyn-related kinase
WNT/β-catenin
Epithelial-mesenchymal transition
title Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p
title_full Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p
title_fullStr Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p
title_full_unstemmed Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p
title_short Nonylphenol promotes epithelial-mesenchymal transition in colorectal cancer cells by upregulating miR-151a-3p
title_sort nonylphenol promotes epithelial mesenchymal transition in colorectal cancer cells by upregulating mir 151a 3p
topic Nonylphenol
Colorectal cancer
microRNA-151a-3p
Fyn-related kinase
WNT/β-catenin
Epithelial-mesenchymal transition
url https://doi.org/10.1007/s12672-025-01805-y
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