Investigation of the relations between miRNA expression profiles and genetic parameters in neuroblastoma cell lines

Despite no gene being identified that is compatible with the double hit hypothesis and the observation of frequent structural and numerical chromosomal aberrations in neroblastoma genetics in areas that are encounter deletion in neuroblastoma; the rare appearance of genetic mutations has led to the recent research of epigenetic changes. The fact that no mutations (excluding Phox2B) have been found in the genes that play a role in the transformation process of neural crest cells and no transcriptional epigenetic change has been determined in the studies that have been done to date on neuroblastoma examples suggests that these genes are able to be silenced with post-transcriptional epigenetic mechanisms. The main objective of our study is to determine the miRNA expression profiles between the cell lines that have 11q and 1p deletion, where deletion is frequently observed during neuroblastoma and the cell lines in which deletion is not observed and to determine whether the genes that play a role in the pathway of neural crest differentiation are the target of miRNA?s in which expression change is observed. In our study, we determined the chromosomal aberrations of the six neuroblastoma cell lines using the MLPA technique. We carried out the miRNA expression profiles of cell lines with an miRNA array study. As a result of our study we determined that in cell lines with 1p deletion show a statistically significant increase in contract to cell lines without 1p deletion of 33 miRNA. We showed that from among these miRNA?s miR-410, miR-543, miR-495 and miR-494 target at least 3 genes. We confirmed the expression increases of miR-543, miR-495 and miR-494, from the selected miRNAs, with a real time PCR study. In conclusion: we believe that the 1p deletion that is frequently observed in neuroblastoma will shed light on the reason for the appearance of neuroblastoma for which the carcinogenesis process is unknown.