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    2021-03-03


    Conflicts of interest
    The authors have no conflict of interest.
    Acknowledgement
    The authors would like to thank Dr. David Weaver and Allen Schroering for their technical support.
    This study was supported by grants from the Moss Foundation and the Hirshberg Foundation for Pancreatic Cancer Research Fund No 58792, USA.
    Appendix A. Supplementary data
    References
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    Contents lists available at ScienceDirect
    Toxicology in Vitro
    journal homepage: www.elsevier.com/locate/toxinvit
    Bisphenol S (BPS) triggers the migration of human non-small cell lung cancer Calcipotriol via upregulation of TGF-β 
    T
    Peng Songa, Kaijie Fanb, , Xiaodong Tianb, Jiaxin Wenb
    a Department of Interventional Radiology, National Cancer Center, National Research Center for Cancer, Cancer Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100021, China b Department of Thoracic Surgery, Chinese PLA General Hospital, Beijing 100853, China
    Keywords:
    BPS
    NSCLC
    Migration TGF-β Smad-2/3 
    As one of the leading causes of cancer deaths world-wide, the progression of human non-small cell lung cancer (NSCLC) can be regulated by estrogenic signals. Our present data showed that an industrial endocrine disrupting chemical, bisphenol S (BPS), can promote the in vitro migration of NSCLC cells, which was evidenced by the upregulation of vimentin and matrix metalloproteinase-2 (MMP-2). BPS can increase the mRNA and protein expression of IL-10 and TGF-β. While only targeted inhibition of TGF-β can block BPS induced migration of NSCLC cells. The upregulation of TGF-β can further activate the Smad-2/3 pathways. Further, BPS induced expression of TGF-β was ERα/β or G protein-coupled estrogen receptor (GPER) independent, since targeted inhibition of ERα/β or GPER had no effect on BPS induced transcription of TGF-β. We identified that the in-hibitor of ERK1/2 can attenuate BPS induced expression of TGF-β and activation of Smad-2/3 pathways. Collectively, we found that nanomolar BPS can trigger the in vitro migration of NSCLC cells via ERK1/2 mediated activation of TGF-β/Smad-2/3 pathways.
    1. Introduction
    Endocrine disrupting compounds (EDCs) are environmental com-pounds which can impact human health through disruption of hormone functions (Henley and Korach, 2006). Bisphenol A (BPA), which has been widely used to produce polycarbonates, is a typical EDC accu-mulated in human body in the diet and through skin contact (Lu et al., 2013). Due to various studies confirmed the negative effects of BPA on human health, BPA has been banned from many human consumer products such as baby's bottles and beverage containers. Bisphenol analogs such as bisphenol S (BPS) are used as substitutes for industrial application (Rochester and Bolden, 2015). However, epidemiological studies suggested that BPS can also accumulate in human body through ingestion and daily exposure (Wu et al., 2018). For example, BPS has been detected in 78% urine samples collected in 2009–2012 from adults in the United States with the median concentration of 0.13 ng/ml (Zhou et al., 2014), which is comparable with the concentrations of BPA in human body. It suggestes that biological safety of BPS is an urgent issue for public health (Rochester and Bolden, 2015).
    Recently, many studies suggested that BPS can also exhibit EDC's effect to modulate various biological functions (Rochester and Bolden, 2015). For example, BPS can increase the rate of adipocyte