<i>In silico</i> analysis demonstrated that none of the miR-221 target genes belonged to heme biosynthetic processes found altered in children with neuroblastoma, whereas two genes associated with mitochondria.
In addition, overexpression of miR-221 decreased LEF1 phosphorylation but increased the expression of MYCN via targeting of NLK and further regulated cell cycle, particularly in S-phase, promoting the growth of neuroblastoma cells.<b>Conclusions:</b> This study provides a novel insight for miR-221 in the control of neuroblastoma cell proliferation and tumorigenesis, suggesting potentials of miR-221 as a prognosis marker and therapeutic target for patients with MYCN overexpressing neuroblastoma.<i></i>.