Exposure of these NB cell lines to 100 μM of harmine resulted in caspase-3/7 and caspase-9 activation as well as caspase-mediated PARP cleavage and Annexin V-positive stained cells, as early as 24 h after treatment, clearly suggesting apoptosis induction, especially in <i>MYCN</i>-amplified cell lines.
Analysis of the CASP9 mediated route in a series of neuroblastoma cell lines, we found normal expression and no aberrant methylation of four apoptotic intermediates, including CASP9 itself.
This suggests that a second, smaller sub-group of MYCN amplified neuroblastoma tumors exists with defect(s) in apoptotic signaling components upstream of caspase-9 and Apaf-1.
We conclude that although coding mutations of Caspase-9 and DFF45 are infrequent in neuroblastoma tumours, our discovery of a rare allele in two neuroblastoma cases should be taken to warrant further studies of the role of DFF45 in neuroblastoma genetics.
We conclude that although coding mutations of Caspase-9 and DFF45 are infrequent in neuroblastoma tumours, our discovery of a rare allele in two neuroblastoma cases should be taken to warrant further studies of the role of DFF45 in neuroblastoma genetics.
Here, we report that human astrocytoma and neuroblastoma cell lines strongly express caspase 9 and 9S mRNA, whereas non-neoplastic human astrocytes show little caspase 9 and 9S mRNA expression.