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Background  Neuroblastoma is a solid tumour of childhood often with an unfavourable outcome. One common genetic feature in aggressive tumours is 1p-deletion.  The α-enolase ( ENO1 ) gene is located in chromosome region 1p36.2, within the common region of deletion in neuroblastoma. One alternative translated product of the  ENO1  gene, known as  MBP-1 , acts as a negative regulator of the  c-myc  oncogene, making the  ENO1  gene a candidate as a tumour suppressor gene.    Methods  Methods used in this study are transfection of cDNA-vectors and  in vitro  transcribed mRNA, cell growth assay, TUNEL-assay, real-time RT-PCR (TaqMan) for expression studies, genomic sequencing and DHPLC for mutation detection.    Results  Here we demonstrate that transfection of  ENO1  cDNA into 1p-deleted neuroblastoma cell lines causes' reduced number of viable cells over time compared to a negative control and that it induces apoptosis. Interestingly, a similar but much stronger dose-dependent reduction of cell growth was observed by transfection of  in vitro  transcribed  ENO1  mRNA into neuroblastoma cells. These effects could also be shown in non-neuroblastoma cells (293-cells), indicating  ENO1  to have general tumour suppressor activity.  Expression of  ENO1  is detectable in primary neuroblastomas of all different stages and no difference in the level of expression can be detected between 1p-deleted and 1p-intact tumour samples. Although small numbers (11 primary neuroblastomas), there is some evidence that Stage 4 tumours has a lower level of  ENO1 -mRNA than Stage 2 tumours (p = 0.01). However, mutation screening of 44 primary neuroblastomas of all different stages, failed to detect any mutations.    Conclusion  Our studies indicate that  ENO1  has tumour suppressor activity and that high level of  ENO1  expression has growth inhibitory effects.

Introduction of in vitro transcribed ENO1 mRNA into neuroblastoma cells induces cell death