Fig. 4.

TriCurin treatment causes an induction in P-NF-KB (P-p65) in the TAM. TC-1 tumor sections parallel to those used in Supplementary Fig. 1 were stained to determine the levels of NF-kB (p65) and activated NF-kB p65 (P-Ser²⁷⁶-p65) in the tumors from Vehicle-treated and TriCurin-treated mice. a Upper and middle rows and b the Vehicle-treated mice displayed basal levels of activated NF-kB p65 (P-Ser²⁷⁶-p65) in the iba1+ TAM, which was increased by 2071% in the TriCurin-treated TC-1 tumor sections (p = 4.20 × 10⁻³). This overall increase of P-NF-kB (P-p65) was a result of c induction of NF-kB (p65) expression (NF-kB (p65) normalized to HOECHST) and d NF-kB (p65) activation (P-NF-kB (P-p65) normalized to NF-kB (p65)). Four randomly chosen sections per mouse were used for imaging and the data (mean ± SEM) compared between Vehicle-treated and TriCurin-treated groups (n = 4 per group). (Scale bar: 47.62 µm). a lower row, showed the lack of non-specific staining from the secondary antibodies (see “Materials and methods”)