Primary cells suppress oncogene-dependent apoptosis
Primary cells suppress oncogene-dependent apoptosis
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DOI：
10.1038/35041112
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发表时间：
2000-11-01
影响因子：
21.3
通讯作者：
Lazebnik, YA
中科院分区：
文献类型：
--
作者：
Duelli, DM;Lazebnik, YA
促进细胞周期进程的癌基因也使细胞对诱导凋亡的药物敏感。致敏被认为是由促凋亡因子的诱导引起的。另外，敏化可能需要通常提供防止细胞死亡保护的失活抑制剂。在这里，我们表明腺病毒癌基因EIA通过至少两种途径使细胞对抗癌药物敏感。一种途径建立了药物与促凋亡因子之间的联系，但如果没有第二种途径（抑制凋亡抑制剂），则不足以致敏。
Oncogenes that promote cell-cycle progression also sensitize cells to agents that induce apoptosis. Sensitization is thought to be caused by the induction of proapoptotic factors. Alternatively, sensitization may require the inactivation inhibitors that ordinarily provide protection against cell death. Here we show that the adenoviral oncogene EIA sensitizes cells to an anti-cancer drug by at least two pathways. One establishes a link between the drug and pro-apoptotic factors, but is not sufficient for sensitization without the second pathway, which suppresses inhibitors of apoptosis.