Fig. 5

The increased 11-HETE counteracted the benefits from reduced EETs caused by PPARα activation on tumour treatment. a A schematic diagram showing the relationship between EETs and 11-HETE and how it is regulated by AVE8134. b ΔEETs and Δ11-HETE represents the difference between EETs and 11-HETE between PPARα ligand-treated groups and the control group. Shown is the correlation between ΔEETs - Δ11-HETE concentration and tumour volume. c1 and c2 Images of TC-1 primary xenograft tumours and their growth curves in WT and Cyp2c44^−/− mice treated with or without AVE8134 (n = 6–7). ^*P < 0.05 vs WT placebo group; ^#P < 0.05 vs WT AVE group; ^&P < 0.05 vs Cyp2c44^−/− placebo group. d and e Levels of EETs and 11-HETE in TC-1 tumours (n = 6–7). ^*P < 0.05 vs WT placebo group; ^#P < 0.05 vs Cyp2c44^−/− placebo group. f1–g2 Representative images of capillary-like structures and cell migration at the indicated treatment and their histograms (n = 7). ^*P < 0.05 vs control; ^#P < 0.05 vs lipo2000; ^&P < 0.05 vs si-nc; ^$P < 0.05 vs si-Cyp2c9. (H) Proliferative ability of HUVECs transfected with Cyp2c9 siRNA and then treated with or without AVE8134, as assessed by BrdU incorporation (n = 4). ^*P < 0.05 vs control; ^#P < 0.05 vs lipo2000; ^&P < 0.05 vs si-nc; ^$P < 0.05 vs si-Cyp2c9. i and j Levels of EETs and 11-HETE in HUVECs transfected Cyp2c9 siRNA and then treated with or without AVE8134 (n = 5). ^*P < 0.05 vs si-nc; ^#P < 0.05 vs si-Cyp2c9