期刊
JOURNAL OF NEUROCHEMISTRY
卷 84, 期 2, 页码 273-281出版社
WILEY
DOI: 10.1046/j.1471-4159.2003.01522.x
关键词
apoptosis; Bcl-2; Bcl-x; bispecific antisense oligonucleotide; brain tumor; glioblastoma
资金
- NINDS NIH HHS [R01 NS29477] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS029477] Funding Source: NIH RePORTER
The functions of the antiapoptotic proteins Bcl-2 and Bcl-xL were examined in glioblastoma. cells, Expression of both Bcl-2 and Bcl-xL were found to be elevated in protein lysates from seven early passage cell lines derived from human glioblastoma tumors compared with non-neoplastic glial cells. Downregulation of both bcl-2 and bcl-xL expression in glioblastoma cell lines U87 and NS008 with bcl-2/bcl-xL bispecific antisense oligonucleotide resulted in spontaneous cell death. The mechanism of cell death was partially caspase-dependent. Executioner caspase 6 and caspase 7, but not caspase 3, were involved in apoptosis induced by bcl-2/bcl-xL antisense treatment. Interestingly, western blots failed to demonstrate expression of caspase 3 in two of the seven glioblastoma cell lines examined. The data support the hypothesis that Bcl-2 and Bcl-xL are important in preventing cell death in glioblastoma cells. It also suggests that there are functional pathways capable of successful completion of caspase-dependent cell death in gliomas. These findings support a potential role of bcl-2/bcl-xL bispecifc antisense oligonucleotide therapy as a treatment strategy to enhance caspase-dependent cell death in patients with glioblastoma.
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