Fig. 2.

EDPs inhibit primary tumor growth. (A) Coadministration of 19,20-EDP (0.05 mg⋅kg⁻¹⋅d⁻¹) and sEHi t-AUCB (1 mg⋅kg⁻¹⋅d⁻¹) suppressed Met-1 breast tumor growth (Ctrl: n = 9 mice per group; 19,20-EDP: n = 8; t-AUCB: n = 5; 19,20-EDP + t-AUCB: n = 11). (Left) Quantification of tumor volume. (Right) Quantification of tumor weight on day 12 of treatment. (B) Analysis of 19,20-EDP in the plasma and tumors of treated mice, coadministration of t-AUCB stabilized 19,20-EDP in vivo. (C) The sEH-metabolite of 19,20-EDP, 19,20-DiHDPA, had no effect on Met-1 tumor growth in mice (n = 4 mice per group). (Right) sEH-dependent metabolic pathway of 19,20-EDP to 19,20-DiHDPA. (D) Contrary to the effect of 19,20-EDP, coadministration of 14,15-EET (0.05 mg⋅kg⁻¹⋅d⁻¹) and sEHi t-AUCB (1 mg⋅kg⁻¹⋅d⁻¹) increased Met-1 tumor growth (n = 6–7 mice per group). (Right) sEH-dependent metabolic pathway of 14,15-EET to 14,15-DHET. (E) Coadministration of 19,20-EDP and t-AUCB reduced tumor vessel density, as defined by the number of CD31-positive blood vessels. (Upper) Image of representative immunohistochemistry for CD31; (Lower) Quantification of tumor vessel density (n = 4 mice per group). Results are presented as means ± SD. *P < 0.05; **P < 0.01; ^#P < 0.001.