Evidence is growing that the $GABA_B$ receptor, which belongs to the G protein-coupled receptor (GPCR) superfamily, is involved in tumorigenesis. Recent studies have shown that ${eta}$-arrestin can serve as a scaffold to recruit signaling protein c-Jun N-terminal knase (JNK) to GPCR. Here we investigated whether ${eta}$-arrestin recruits JNK to the $GABA_B$ receptor and facilitates its activation to affect the growth of cancer cells. Our results showed that ${eta}$-arrestin expression is decreased in breast cancer cells in comparison with controls. ${eta}$-arrestin could enhance interactions of the $GABA_BR{cdot}{eta}-arrestin{cdot}JNK$ signaling module in MCF-7 and T-47D cells. Further studies revealed that increased expression of ${eta}$-arrestin enhances the phosphorylation of JNK and induces cancer cells apoptosis. Collectively, these results indicate that ${eta}$-arrestin promotes JNK mediated apoptosis via a $GABA_BR{cdot}{eta}-arrestin{cdot}JNK$ signaling module.