Bisphenol A at a human exposed level can promote epithelial‐mesenchymal transition in papillary thyroid carcinoma harbouring BRAFV600E mutation. Issue 3 (19th January 2021)

• Record Type: Journal Article
• Authors: Li, Liuli; Li, Hao; Zhang, Jun; Gao, Xin; Jin, Hao; Liu, Renqi; Zhang, Zhen; Zhang, Xuan; Wang, Xichang; Qu, Peng; Zhao, Yuejiao; Lu, Xiaobo
• Is Part Of: Journal of cellular and molecular medicine. Volume 25:Issue 3(2021)
• Page Start: 1739
• Page End: 1749
• Publication Date: 2021-01-19
• Subjects: Bisphenol A -- BRAFV600E mutation -- epithelial‐mesenchymal transition -- ERK‐Cox2 -- Papillary thyroid carcinoma; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.16279
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Bisphenol A (BPA), a ubiquitous endocrine‐disrupting chemical, alters the function of endocrine system and enhances the susceptibility to tumorigenesis in several hormone‐dependent tumours as thyroid carcinoma. About 50% of papillary thyroid cancers (PTC), the most common type of thyroid malignancy, harbours the BRAF V600E mutation. This study aimed to investigate a potential combined effect of BPA exposure and BRAF V600E mutation on epithelial‐mesenchymal transition (EMT) in PTC. Firstly, the level of BPA in plasma, the evaluation of BRAF V600E mutation and the level of EMT‐related proteins in PTC samples were individually determined. Additionally, the migration, invasion, colony formation capacity and the expression of EMT‐related proteins after exposure to BPA were precisely analysed in vitro thyroid cells genetically modified by the introduction of BRAF V600E mutation. Moreover, ERK‐Cox2 signalling pathway was also introduced to explore the possible mechanism in PTC development. As expected, whether the clinical investigation or cultured thyroid cells demonstrated that BPA at a concentration compatible with human exposed levels (10 ‐7 M) synergized with the BRAF V600E mutation promoted EMT via the activation of ERK‐Cox2 signalling pathway. Our findings offer some evidence that BPA as an environmental risk factor can facilitate the progression of PTC harbouring BRAF V600E mutation.