Fig. 4.

PRL3-zumab eliminates tumors in an Fc- and FcR-dependent manner. a Cartoon depicting domain architecture of PRL3-zumab (intact Fc) vs. PRL3-minibody (truncated Fc lacking CH1 and CH2 domains) and their ability to engage Fc receptors (FcR) on host immune cells. The anti-CD16/32 FcR blocker antibody prevents IgG from binding murine FcγII/III receptors. b Both Fc region of PRL3-zumab and FcR binding are required for anti-tumor effects of PRL3-zumab. Upper panel, representative images of livers from each treatment group at day 35 (5-week endpoint). Tumor areas are framed with black lines. Scale bar, 10 mm. Lower panel, tumor volumes in each group. The mean tumor volumes were calculated using one-way analysis of variance (ANOVA) (mean ± s.e.m.) for independent groups of untreated (n = 12), human IgG-treated (n = 3), PRL3-zumab-treated (n = 6), PRL3-minibody-treated (n = 5), PRL3-zumab + FcR blocked-treated (n = 7), and FcR blocker-treated (n = 4) mice. Source data are provided as a Source Data file