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Transcription factor activity of estrogen receptor α activation upon nonylphenol or bisphenol A treatment enhances the in vitro proliferation, invasion, and migration of neuroblastoma cells

Authors Ma H, Yao Y, Wang C, Zhang L, Cheng L, Wang Y, Wang T, Liang E, Jia H, Ye Q, Hou M, Feng F

Received 3 February 2016

Accepted for publication 11 March 2016

Published 13 June 2016 Volume 2016:9 Pages 3451—3463

DOI https://doi.org/10.2147/OTT.S105745

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Triparna Sen

Peer reviewer comments 2

Editor who approved publication: Dr William Cho


Hongda Ma,1 Yao Yao,2 Changli Wang,1 Liyu Zhang,3 Long Cheng,4 Yiren Wang,5 Tao Wang,6 Erguang Liang,6 Hui Jia,1 Qinong Ye,4 Mingxiao Hou,1 Fan Feng1

1Department of Pharmacy, General Hospital of Shenyang Military Area Command, Shenyang, 2Department of Pharmacy, Women & Infants Hospital of Zhengzhou, Zhengzhou, 3Shaanxi Institute of Pediatric Disease, Xi’an Children’s Hospital, Xi’an, 4Institute of Biotechnology, Chinese Military Medical Science Academy, Beijing, 5School of Life Science, Shenyang Pharmaceutical University, Shenyang, 6Institute of Toxicology and Pharmacology, Chinese Military Medical Science Academy, Beijing, People’s Republic of China

Abstract: Many kinds of endocrine-disrupting chemicals (EDCs), for example, the environmental estrogens bisphenol A and nonylphenol, may regulate the activity of estrogen receptor α (ERα) and therefore induce potential disruption of normal endocrine function. However, the involvement of EDCs in human cancers, especially in endocrine-related cancer neuroblastoma regulation, is not very clear. In this work, results showed that upon bisphenol A or nonylphenol treatment, the transcription factor activity of ERα was significantly increased in neuroblastoma cell line SH-SY5Y. Bisphenol A and nonylphenol could enhance ERα activity via recruiting it to the target gene promoter. Furthermore, treatment of bisphenol A and nonylphenol enhanced the in vitro proliferation, invasion, and migration ability of neuroblastoma cells. By investigating the role of EDC-induced ERα upregulation, our data extend the understanding of the function of EDCs and further suggest that ERα might be a potential therapeutic target in human neuroblastoma treatment.

Keywords: neuroblastoma, endocrine-disrupting chemicals, environmental estrogens, bisphenol A and nonylphenol, proliferation and metastasis

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