Fig 1: JAK2/STAT3 signaling pathway was related to C3 deposition in GC tissues and C3-induced oncoprogression. a Typical expression of p-STAT3 and IL-6 in GC and adjacent normal tissues (IFC method), which indicates an up-regulation of STAT3 signaling in GC patients (representative images of n = 5 independent experiments); b Levels of JAK2/STAT3-related proteins (IL-6, p-JAK2, p-STAT3 and STAT3) were detected on SGC-7901 and normal GES-1 cell line with WB method (left panel). The STAT3 signaling was highly activated with exogenous C3 treatment, and greatly inhibited when JAK2-blocker (AG490) was pre-incubated with C3 (right panel); c Levels of p-STAT3 and IL-6 in C3-antagonist pre-treated GC cells (upper panel). The JAK2/STAT3 signaling remained activated but weakened under blockage of C3 signaling with CR1 compared with blockage of JAK2 with AG490 (lower panel). 20,000 cells per sample in all in vitro assays, representative histograms (right panel) of n = 5 independent experiments; d A proposed model for the underlying mechanism of C3/JAK2/STAT3 signaling pathway participating in the pathogenesis of GC. Abbreviations: 3aR, Complement C3a receptor; MAC, membrane attack complex; CVF, cobra venom factor