TY - JOUR
T1 - GPER/Hippo-YAP signal is involved in Bisphenol S induced migration of triple negative breast cancer (TNBC) cells
AU - Deng, Qianqian
AU - Jiang, Guanmin
AU - Wu, Yingmin
AU - Li, Jiexin
AU - Liang, Weiting
AU - Chen, Likun
AU - Su, Qiao
AU - Li, Wuguo
AU - Du, Jun
AU - WONG, Chris K C
AU - Chen, Zhuojia
AU - Wang, Hongsheng
N1 - Funding Information:
This research was supported by the National Natural Science Foundation of China (Grant No. 81673454 , No. 81672608 , No. 81472470 , and No. 81572270 ), the Guangdong Natural Science Funds for Distinguished Young Scholar (No. 2014A030306025 ), the Pearl River S&T Nova Program of Guangzhou (No. 1517000390 ), the Fundamental Research Funds for the Central Universities (Sun Yat-sen University) ( 16ykpy09 ), the Guangdong Province Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation (No. 2017B030314026 ), and the Science & Technology Planning Project of Guangdong Province ( 2014A030304016 , 2017A030303015 ). Appendix A
PY - 2018/8/5
Y1 - 2018/8/5
N2 - 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.
AB - 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.
KW - Bisphenol S
KW - GPER
KW - migration
KW - TNBC
KW - YAP
UR - http://www.scopus.com/inward/record.url?scp=85046755478&partnerID=8YFLogxK
U2 - 10.1016/j.jhazmat.2018.05.013
DO - 10.1016/j.jhazmat.2018.05.013
M3 - Article
C2 - 29758456
AN - SCOPUS:85046755478
SN - 0304-3894
VL - 355
SP - 1
EP - 9
JO - Journal of Hazardous Materials
JF - Journal of Hazardous Materials
ER -
