| Literature DB >> 29758456 |
Qianqian Deng1, Guanmin Jiang2, Yingmin Wu1, Jiexin Li1, Weiting Liang3, Likun Chen3, Qiao Su4, Wuguo Li4, Jun Du1, Chris K C Wong5, Zhuojia Chen6, Hongsheng Wang7.
Abstract
Nowadays, risk factors of triple-negative breast cancer (TNBC) metastasis are not well identified. Our present study reveals that an industrial chemical, bisphenol S (BPS), can promote the migration, but not the proliferation, of TNBC cells in vitro. BPS activates YAP, a key effector of Hippo pathway, by inhibiting its phosphorylation, which promotes YAP nuclear accumulation and up-regulates its downstream genes such as CTGF and ANKRD1. Inhibition of YAP blocks the BPS-triggered cell migration and up-regulation of fibronectin (FN) and vimentin (Vim). BPS rapidly decreases the phosphorylation levels of LATS1 (Ser909) in TNBC cells, which regulates the activation and functions of YAP. Silencing LATS1/2 by siRNA increases BPS-induced dephosphorylation of YAP and extended the half-life of YAP protein. Inhibition of G protein-coupled estrogen receptor 1 (GPER) and its downstream PLCβ/PKC signals attenuate the effects of BPS-induced YAP dephosphorylation and CTGF up-regulation. Targeted inhibition of GPER/YAP inhibits BPS-induced migration of TNBC cells. Collectively, we reveal that GPER/Hippo-YAP signal is involved in BPS-induced migration of TNBC cells.Entities:
Keywords: Bisphenol S; GPER; TNBC; YAP; migration
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Year: 2018 PMID： 29758456 DOI： 10.1016/j.jhazmat.2018.05.013
Source DB: PubMed Journal: J Hazard Mater ISSN： 0304-3894 Impact factor: 10.588