Fig. 4: CSF1R inhibition reduces PCa tumor burden but potentiates pro-tumorigenic signatures.
From: S-nitrosylation of CSF1 receptor increases the efficacy of CSF1R blockage against prostate cancer
A Representative bright-field, H and E and immunofluorescent images for 22Rv1 derived organoids stained with 4′,6-diamidino-2-phenylindole (DAPI) (blue) and Cysteine sulfinic acid (red) showing oxidation status. The chromogenic substrate DAB (brown) represents the expression of NOS3 in untreated control and CSF1Ri treated organoids. Scale bar 400 μm. B Experimental plan. C Mean change of tumor volume (±SEM; versus tumor volume at treatment start) in C5BL6 mice treated as indicated. Vehicle (n = 5), α-CSF1R (n = 5). Animal weight changes throughout the experiment from Day 1 to Day 28. Tumor weight plotted as Mean ± SEM (n = 5) measured at the end of the experiment. D GSNOR activity was measured at 340 nm for 10 minutes using tumor lysates treated with vehicle and CSF1R inhibitor (n = 3). E Representative immunofluorescent images for tumor sections for mice treated with vehicle and CSF1R inhibitor and stained with 4′,6-diamidino-2-phenylindole (DAPI) (blue) and Cysteine sulfinic acid (red) (n = 3). F Representative tSNE plots and graphs for various immune cell surface markers (TCRβ, CD19, CD11b, iNOS, and CD206) for tumor cells isolated from mice tumors treated with vehicle and CSF1R inhibitor.
