Fig. 4

LIF-neutralizing antibody acts as a therapeutic approach for treating KRAS-driven pancreatic cancers. a Representative ELISA assay showing that LIF antibodies (D25.1.4 and D62.3.2) prevent recombinant human LIF from binding to microplate pre-coated with human LIF monoclonal antibody (Invitrogen BMS242). b Representative western blots suggesting that use of a LIF-neutralizing antibody blocks the STAT3 activation/phosphorylation induced by recombinant human LIF (50 ng/mL) in human pancreatic cancer cell lines, whereas IL-6 induces STAT3 activation. c Tumor free survival rate and numbers of palpable tumors in Panc2.03 xenografts model receiving control or LIF antibody at 10 mg/kg. (d) Tumor growth in syngeneic mouse model receiving gemcitabine (50 mg/kg), LIF antibody (20 mg/kg), or gemcitabine along with LIF antibody. The cancer cells are expressed with firefly luciferase, which can be used to detect orthotopic tumor growth. Twice a week of treatments started on the fourteenth day post-tumor cell injections (N = 5, ****P < 0.0001). e Overall survival rate of syngeneic mouse model receiving gemcitabine, LIF antibody, or gemcitabine along with LIF antibody. f Tumor growth curve of PDX (patient-derived xenograft)_PC105 receiving gemcitabine (100 mg/kg) or gemcitabine along with LIF antibody (10 mg/kg). The treatment of gemcitabine was conducted once a week and LIF antibody was authorized twice a week (N = 6, *P < 0.05). g Tumor growth curve of PDX_PC187 receiving control IgG, gemcitabine (100 mg/kg), LIF antibody (10 mg/kg), or gemcitabine along with LIF antibody (10 mg/kg). The treatment of gemcitabine was conducted once a week and LIF antibody was authorized twice a week (N = 7, *P < 0.05; **P < 0.01). d, f, g Error bars: mean ± SEM and P-value was generated by Two-way ANOVA