Glial-specific retrovirally mediated gas1 gene expression induces glioma cell apoptosis and inhibits tumor growth in vivo.
We recently reported that the targeted expression of growth arrest specific 1 ( Gas1) induces apoptosis in glioma cells. Because the vast majority of gliomas present genetic alterations that reduce their ability to undergo apoptosis, a gene therapy strategy aimed at reinstating apoptotic processes in glioma cells is an interesting approach for the treatment of these tumors. We used a retroviral gene transfer system to transduce C6 glioma cells with a transgene in which the expression of a full-length human gas1 cDNA is under the transcriptional control of a human promoter of the glial fibrillary acidic protein ( gfa2). In vitro experiments showed that the retroviral transfer of gas1 significantly reduces the number of viable cells, and induces apoptosis in C6 cells, through the activation of caspase-3. Furthermore, retroviral-mediated transfer of gas1 to gliomas implanted in nude mice induces a significant inhibition of tumor growth, accompanied by increased caspase-3 activation. In the present experiments, we have taken advantage of the property of retrovirus to transfer transgenes exclusively to proliferating cells, together with the use of a glial specific promoter, to selectively target the expression of gas1, a pro-apoptotic gene, to glioma cells.[1]References
- Glial-specific retrovirally mediated gas1 gene expression induces glioma cell apoptosis and inhibits tumor growth in vivo. Zamorano, A., Mellström, B., Vergara, P., Naranjo, J.R., Segovia, J. Neurobiol. Dis. (2004) [Pubmed]
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