Fig. 4

11-HETE promoted endothelial proliferation and angiogenesis, causing tumour growth and lung metastasis. a1 and a2 Images of TC-1 primary xenograft tumours and their growth curves in mice treated with or without 11-HETE (n = 8). ^*P < 0.05 vs control. b1 and b2 Hematoxylin and eosin (HE) staining and the number of lung metastatic tumours (red arrowhead; n = 8). ^*P < 0.05 vs control. c The weight of lungs in TC-1 tumour-bearing mice (n = 8). ^*P < 0.05 vs control. d1 and d2 Tumour vascularization was quantified by CD31 antibodies in paraffin sections of TC-1 primary xenograft tumours (n = 8). ^*P < 0.05 vs control. e1 and e2 Images of B16F10 primary xenograft tumours and their growth curves in mice treated with or without 11-HETE (n = 8). ^*P < 0.05 vs control. f and g Levels of EETs and 11-HETE in TC-1 tumours of treated mice. ^*P < 0.05 vs control. h Proliferative ability of HUVECs treated with EETs and different doses of 11-HETE, as assessed by BrdU incorporation (n = 4). ^*P < 0.05 vs. control. i1 and i2 Representative images of migrated cells at the indicated treatment (n = 10). ^*P < 0.05, vs control. j1 and j2 Representative images of capillary-like structures at the indicated treatment (n = 7). ^*P < 0.05 vs control. k1–l2 Western blot showing the activation of the AKT and ERK pathways under 11-HETE stimulation (n ≥ 3). *P < 0.05 vs control