Concurrent activation of β₂-adrenergic receptor and blockage of GPR55 disrupts pro-oncogenic signaling in glioma cells.

ABSTRACT: Activation of β₂-adrenergic receptor (β₂AR) and deorphanized GPR55 has been shown to modulate cancer growth in diverse tumor types in vitro and in xenograft models in vivo. (R,R')-4'-methoxy-1-naphthylfenoterol [(R,R')-MNF] is a bivalent compound that agonizes β₂AR but inhibits GPR55-mediated pro-oncogenic responses. Here, we investigated the molecular mechanisms underlying the anti-tumorigenic effects of concurrent β₂AR activation and GPR55 blockade in C6 glioma cells using (R,R')-MNF as a marker ligand. Our data show that (R,R')-MNF elicited G1-phase cell cycle arrest and apoptosis, reduced serum-inducible cell motility, promoted the phosphorylation of PKA target proteins, and inhibited constitutive activation of ERK and AKT in the low nanomola

SUBMITTER: Wnorowski A 

PROVIDER: S-EPMC5512002 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature