The role of epigenetics and miRNAs in neuroblastoma development

Introduction Neuroblastoma (NB) is an often fatal pediatric cancer that arises from the precursor cells of the sympathetic nervous system. 13-Cis retinoic acid is used to treat high-risk disease. A derivative, all-trans-retinoic acid (ATRA) causes genome-wide demethylation in NB cells by up-regulating miRNAs such as miR-152 and miR-26a/b which are predicted to target the methyltransferases DNMT1 and DNMT3b, respectively. The purpose of this study was to test whether ectopic over-expression of miR-26a/b, a known tumor suppressor miRNA in several other cancer types, led to reduced cell viability and DNMT3b expression in SK-N-BE NB cells. In addition, we also carried out a methylated DNA immunoprecipitation to microarrays following miR-152 over-expression in SK-N-BE cells in order to assess whether the ectopic over expression of miR-152 had any effects on genome-wide methylation.