Corilagin blocks multiple signaling pathways. (A) RPPA analysis of untreated and Corilagin (at lower, 20 μM, and higher, 40 μM, concentrations)-treated HO8910PM cells. Figure presents a small portion of the results. (B) Corilagin inhibited pAKT, Myt1 and pERK in Hey, SKOv3ip, or HO8910PM cells. Non-phosphorylated AKT, GAPDH and non-phosphorylated ERK were used as the loading controls. (C) Corilagin (as compound C) inhibited AKT signaling in Hey cells, but ethyl brevifolin carboxylate (as compound A) did not. Non-phosphorylated AKT was used as the loading control. (D) Corilagin inhibited the expression of pERK and Snail in HO8910PM-Snail cells and the TGF-β-mediated stimulation of pERK and Snail. Non-phosphorylated ERK was used as the loading control. U126, a pERK inhibitor, was used as the positive control. (E) Corilagin inhibited TGF-β-mediated pSmad2 expression in HO8910PM and SKOv3ip cells. Non-phosphorylated Smad2 was used as the loading control.
Jia et al. BMC Complementary and Alternative Medicine 2013 13:33 doi:10.1186/1472-6882-13-33