Overexpression of E2F1 in glioma-derived cell lines induces a p53-independent apoptosis that is further enhanced by ionizing radiation
Overexpression of E2F1 in glioma-derived cell lines induces a p53-independent apoptosis that is further enhanced by ionizing radiation
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DOI：
10.1093/neuonc/2.1.16
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发表时间：
2000-01-01
期刊：
影响因子：
15.9
通讯作者：
Israel, MA
中科院分区：
文献类型：
--
作者：
Shu, HKG;Julin, CM;Israel, MA
神经胶质瘤细胞系以受 p53 状态影响的方式对辐射表现出不同的反应，神经胶质瘤细胞系的辐射通常不会诱导细胞凋亡，当野生型 p53 存在时，这些细胞会经历 G(1) 停滞，这与通过克隆生存测量的放射敏感性增加密切相关。 此前，其他人已经表明，E2F1 的失调过度表达会诱导具有功能性或失活 p53 的细胞系凋亡。我们发现，无论 p53 状态如何，电离辐射处理进一步增强了神经胶质瘤细胞系中 E2F1 过度表达诱导的细胞凋亡。在测试的神经胶质瘤细胞系中，BAX 诱导并不遵循 E2F1 过表达或辐射。因此，E2F1可以通过不涉及BAX诱导的机制增强神经胶质瘤来源的细胞对辐射的凋亡反应。
Glioma cell lines show variable responses to radiation in a manner influenced by their p53 status, Irradiation of glioma cell lines does not generally induce apoptosis, When wild-type p53 is present, these cells undergo a G(1) arrest that is closely associated with increased radiosensitivity as measured by clonogenic survival, Previously, others have shown that dysregulated overexpression of E2F1 induces apoptosis in cell lines with either functional or inactivated p53, We found that regardless of p53 status, apoptosis induced by overexpression of E2F1 in glioma cell lines was further enhanced by treatment with ionizing radiation. BAX induction did not follow E2F1 overexpression or irradiation in the glioma cell lines tested. Thus, the apoptotic response of glioma-derived cells to irradiation can be enhanced by E2F1 by a mechanism that does not involve the induction of BAX.