Fig. 5

BFE quenched the HGF-enhanced breast cancer aggressiveness through inhibition of c-Met receptor phosphorylation: a the images show the phosphorylation status of c-Met, Stat3 and Jak2; and also the total protein levels of the c-Met receptor and the beta-actin control within the BT549 cell line following SDS-PAGE and Western blotting procedures. The different treatment groups displayed no significant differences when comparing the total protein levels for c-Met and the beta-actin control. Importantly, we show that HGF-stimulation of these cells resulted in a significant increase in activation and phosphorylation of the c-Met receptor. This HGF-enhanced phosphorylation was quenched through the co-incubation of BFE. b The ratio between phosphorylated c-Met and total c-Met was calculated to and plotted to demonstrate that the addition of BFE, rather than aberrant protein levels, was responsible for the shift in receptor phosphorylation status. c Gelatinase Zymography revealed no significant differences in MMP2/9 expression levels within the breast cancer cells following HGF/BFE treatments