Figure 7. Status of N-MYC/Nm23-H1 high and h-Prune NBL tumors and a model of action of CPP.

(a) Level of phosphorylation of Nm23-H1 and complex formation through the h-Prune C-terminal has prognostic relevance for determining an aggressive NBL phenotype, and thus worse outcome. (b) Use of the mimetic peptide CPP which can impair the binding of Nm23-H1 and h-Prune in vitro and in vivo, resulting in substantial impairment of cell motility and metastatic niche formation in vivo, with therapeutic benefit. This is accompanied by inhibition of the WNT, NF-κb, AKT and FAK intracellular signaling pathways.