Induction of apoptosis in T98G glioblastoma cells by transfection of GML, a p53 target gene.
Expression of the glycosyl-phosphatidylinositol-anchored molecule-like protein ( GML) gene, a p53 target, correlates with the sensitivity of some cancer cell lines to anticancer drugs and ionizing radiation. To investigate the function of GML further, we introduced the GML cDNA into various cancer cell lines under control of the tetracycline-regulated system. When we introduced GML into human glioblastoma cell line T98G, which lacks wild-type p53 and expresses no endogenous GML, we observed significant growth suppression accompanied by G2/M arrest in two independent, stable cell lines. We confirmed induction of apoptosis by fluorescence-activated cell sorting (FACS) analysis and nuclear staining. Our results indicated that GML could induce apoptosis of T98G without functional p53, and implied that GML plays a crucial role in the apoptotic pathway in some cancer cells.[1]References
- Induction of apoptosis in T98G glioblastoma cells by transfection of GML, a p53 target gene. Ueda, K., Miyoshi, Y., Tokino, T., Watatani, M., Nakamura, Y. Oncol. Res. (1999) [Pubmed]
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