Modulating Inflammation in Colorectal Cancer

For SP600125 treatment, WT and Rip3^-/- mice were administered the JNK inhibitor SP600125 (40 mg/kg) (Sigma-Aldrich) or vehicle (DMSO) by oral gavage once daily during CAC induction. For anti-CXCL1 treatment, WT and Rip3^-/- mice receiving AOM/DSS were treated either with a mouse anti-CXCL1 neutralizing antibody (120 µg/mouse once a week, i.p.) or mouse IgG1 isotype control (both from R&D Systems) until sacrifice (day 100). For anti-CD90 treatment, T cells were depleted with neutralizing anti-CD90 monoclonal antibody as previously described 23 (link). Rip3^-/- mice receiving AOM/DSS were treated either with a mouse anti-CD90 neutralizing antibody (100 µg/mouse once a week, i.p.) or isotype control (both from BioXcell) until sacrifice (day 100). For recombinant CXCL1 treatment, Rip3^-/- mice receiving AOM/DSS were treated either with mouse recombinant CXCL1 (300 ng/mouse twice a week, i.p.) or control PBS (both from R&D Systems) until sacrifice (day 100).