Fig. 2From: The complement system in glioblastoma multiformeProposed interaction of complement C3a and C5a with GSC regulatory mechanisms. C5a-C5aR interaction activates PI3K/Akt/mTOR signaling and PKCζ but suppresses p21 with subsequent OCT-4 activation. Intracellular activation of C3a by cathepsin-L may occur, thereby sustaining basal mTOR activation. Either intracellular or extracellular derived C3a phosphorylates STAT-3 and causes an increase of SOX-2 expressionBack to article page