Down-regulation of Bcl-2 and Bcl-xL expression with bispecific antisense treatment in glioblastoma cell lines induce cell death.

摘要: The functions of the antiapoptotic proteins Bcl-2 and Bcl-xL were examined in glioblastoma cells. Expression both found to be elevated protein lysates from seven early passage cell lines derived human tumors compared with non-neoplastic glial Down-regulation bcl-2 bcl-xL expression U87 NS008 bcl-2/bcl-xL bispecific antisense oligonucleotide resulted spontaneous death. mechanism death was partially caspase-dependent. Executioner caspase 6 7, but not 3, involved apoptosis induced by treatment. Interestingly, western blots failed demonstrate 3 two examined. data support hypothesis that are important preventing It also suggests there functional pathways capable successful completion caspase-dependent gliomas. These findings a potential role bispecifc therapy as treatment strategy enhance patients glioblastoma.