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. 2016 Jul 20;7(32):52375–52391. doi: 10.18632/oncotarget.10737

Figure 7.

Figure 7

(A) Fluorescence quantitation of NO presence in human (hCMEC) and mouse (sEND1) endothelial cell lines +/− 48 h incubation with VEGF. *p < 0.05. (B) Western-blot showing p53 levels in MDA231Br-GFP cells after 72 h co-culture with hCMEC or sEND1 endothelial cells, respectively, +/− pre-activation of endothelial cells with VEGF. (C) Quantitation of p53 DINP1 levels in MDA231Br-GFP cells. Experiments were run in triplicate and statistical significance determined by t student: *p < 0.05. (D) Schematic illustrating putative activation of LFA-1 signalling pathways during metastatic growth in the brain. (1) The integrin LFA-1 on tumour cells interacts with its cognate ligand ICAM-1 (or alternative ligands ICAM-2, ICAM-3, ICAM-4 and JAM-1) on astrocytes, microglia, neurons and endothelial cells. (2) This interaction supports tumour growth by up-regulating COX-2 expression (predominantly in astrocytes) and consequent release of VEGF. (3) VEGF is taken up by endothelial cells and upregulates expression of endothelial NOS (eNOS). (4) The resultant increase in nitric oxide release impairs p53, potentially leading to enhanced tumour growth.