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. 2012 Feb 15;31(4):786–787. doi: 10.1038/emboj.2011.504

Figure 1.

Figure 1

Loss of miR-126 in cancer cells promotes endothelial cell recruitment through a non-cell autonomous mechanism involving its direct targets. MiR-126 in the cancer cell directly targets MERTK, IGFBP2, and PITPNC1. PITPNC1 promotes secretion of IGFBP2, which binds to IGF1 to facilitate its binding to IGF1R on endothelial cells. MERTK is cleaved and its extracellular domain (ECD) binds GAS6, a MERTK ligand that inhibits endothelial cell recruitment, thereby acting as a GAS6 antagonist to promote endothelial recruitment. MiR-126 in endothelial cells acts in a cell autonomous manner to promote angiogenesis through activation of the PI3K-Akt and RAF-1-ERK pathways. The miR-126 endothelial cell autonomous functions are adapted from Fish et al (2008).