Gaurnier-Hausser A et al. - Angiocidin activates monocytes to secrete cytokines and differentiates them to a macrophage-like phenotype through at least two pathways mediated by MAPK and NF-κB, as well as PI3K. Methods
Angiocidin, a tumor and vascular associated protein, is a potent inhibitor of angiogenesis and tumor growth
This study describes another activity of angiocidin that may contribute to its antitumor activity
Results
Angiocidin activated monocytes to secrete a mixture of proinflammatory cytokines and induced them to differentiate into macrophage-like cells
Angiocidin induced the cells to become adherent and phagocytic, express macrophage markers, and secrete MMP-9
Angiocidin up-regulated p105/p50, p100/p52, and rel B, components of the NF-κB pathway
Angiocidin induced phosphorylation of Iκβ p50, and p65 and translocation of p50 and p65 to the nucleus
Angiocidin activated up-stream mediators of NF-κB, such as the MAPK pathway and PI3K
Blockage of NF-κB and MAPK activation with small molecule inhibitors completely prevented angiocidin-mediated secretion of cytokines from THP-1 cells
However, this did not inhibit their adhesive phenotype
Blocking PI3K inhibited both secretion of cytokines, as well as the adhesive phenotype
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