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. 2015 Sep 8;6(31):31378–31398. doi: 10.18632/oncotarget.5145

Figure 7. Activation of MET signaling in SMS-CTR ERMS cells induces proangiogenic effects in vitro by upregulation of miR-378, VEGF and MMP9, whereas MET silencing in RH30 ARMS exerts the opposite effects.

Figure 7

A. TPR-MET SMS-CTR cells conditioned media increase the amount of junctions, nodes and meshes formed by HUVEC cells in Matrigel angiogenesis assay in vitro, n = 4. B. Expression of VEGF, MMP9, miR-378a-5p and miR-378-3p is increased in SMS-CTR ERMS cells expressing TPR-MET and downregulated in shMET RH30 ARMS cells in vitro, qPCR, n = 2–4. C. Inhibition of miR-378a with anti-miR sequences reverses the effect of TPR-MET on VEGF mRNA and protein, n = 2–4. *p < 0.05, **p < 0.01, ***p < 0.001. Data in graphs are represented as mean +/− SEM.