Huang Y, Ishiko T, Nakada S, Utsugisawa T, Kato T, Yuan Z M
Division of Cancer Pharmacology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Cancer Res. 1997 Sep 1;57(17):3640-3.
Mammalian cells respond to ionizing radiation (IR) with transient cell cycle arrest and induction of apoptosis. Here we show that IR increases the expression of the E2F-1 transcription factor and the entry of cells into S phase. E2F-1 transactivation function is inhibited by cyclin A-kinase to ensure orderly progression through S phase. However, in contrast to proliferating cells, IR treatment results in down-regulation of cyclin A-kinase. Expression of a dominant negative form of the E2F heterodimeric partner DP-1 confirmed the involvement of E2F in IR-induced S-phase entry. These findings also support opposing signals involving the induction of E2F and the down-regulation of cyclin A-kinase in the IR response.
哺乳动物细胞对电离辐射(IR)的反应是短暂的细胞周期停滞和凋亡诱导。我们在此表明,IR会增加E2F-1转录因子的表达,并使细胞进入S期。细胞周期蛋白A激酶会抑制E2F-1的反式激活功能,以确保细胞有序地通过S期。然而,与增殖细胞不同,IR处理会导致细胞周期蛋白A激酶下调。E2F异二聚体伴侣DP-1的显性负性形式的表达证实了E2F参与IR诱导的S期进入。这些发现还支持了在IR反应中涉及E2F诱导和细胞周期蛋白A激酶下调的相反信号。