Lentiviral knockdown of PAR1 inhibited the expansion and self-renewal of human GBM-derived A2B5(+) TPCs in vitro, while pharmacological inhibition of PAR 1 similarly slowed both the growth and migration of A2B5(+) TPCs in culture.
TIC-like cells may play a role in these effects, as they express TF and PAR-1/2, and respond to stimulation with their agonists.As major human malignancies (e.g. glioblastoma) are increasingly recognized to consist of a spectrum of molecularly distinct disease subtypes driven by specific genetic pathways, so too may their patterns of interaction differ with the coagulation system.