GPER/Hippo-YAP signal is involved in Bisphenol S induced migration of triple negative breast cancer (TNBC) cells

Qianqian Deng, Guanmin Jiang, Yingmin Wu, Jiexin Li, Weiting Liang, Likun Chen, Qiao Su, Wuguo Li, Jun Du, Chris K. C. Wong, Zhuojia Chen*, Hongsheng Wang

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

48 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalJournal of Hazardous Materials
Volume355
DOIs
Publication statusPublished - 5 Aug 2018

Scopus Subject Areas

  • Environmental Engineering
  • Environmental Chemistry
  • Waste Management and Disposal
  • Pollution
  • Health, Toxicology and Mutagenesis

User-Defined Keywords

  • Bisphenol S
  • GPER
  • migration
  • TNBC
  • YAP

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