Apoptosis induced in mammalian cells by small peptides that functionally antagonize the Rb-regulated E2F transcription factor
Apoptosis induced in mammalian cells by small peptides that functionally antagonize the Rb-regulated E2F transcription factor
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DOI：
10.1038/nbt0997-896
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发表时间：
1997-09-01
影响因子：
46.9
通讯作者：
LaThangue, NB
中科院分区：
文献类型：
--
作者：
Bandara, LR;Girling, R;LaThangue, NB
各种研究表明E2 F转录因子是哺乳动物细胞周期的关键调节因子。E2 F途径在大多数（如果不是全部的话）人肿瘤细胞中是异常的;因此，调节E2 F活性的治疗方案可以提供在正常生理控制丧失的情况下恢复生长控制的方法。为了阐明E2 F在细胞周期中的作用并评估其作为治疗靶点的价值，我们将功能性拮抗E2 F DNA结合活性的肽引入哺乳动物细胞中。将这些肽引入哺乳动物肿瘤细胞引起细胞凋亡的快速发生，这一结果与生理E2 F的失活相关。
A variety of studies implicate the E2F transcription factor as a critical regulator of the mammalian cell cycle. The E2F pathway is aberrant in most, if not all, human tumor cells; therefore, therapeutic regimes that modulate E2F activity may provide an approach for reinstating growth control in situations where normal physiological control is lost. To elucidate the role of E2F in the cell cycle and assess its value as a therapeutic target, we have introduced peptides that functionally antagonize E2F DNA binding activity into mammalian cells. Introduction of these peptides into mammalian tumor cells caused the rapid onset of apoptosis, an outcome that correlates with the inactivation of physiological E2F.