Goldstone S D, Lavin M F
Department of Pathology, University of Sydney, NSW, Australia.
Oncogene. 1994 Aug;9(8):2305-11.
The product of the c-jun gene is a component of the transcription factor AP-1, which plays a critical regulatory role in the cellular response to certain proliferative stimuli. In this report, we demonstrate the prolonged expression of c-jun mRNA during apoptosis induced in a human leukaemic T-cell line, CEM C7, by treatment with either dexamethasone or gamma-radiation. However, overexpression of the c-jun mRNA was not accompanied by either increased expression of jun protein, or increased AP-1 DNA binding activity. Indeed, a decrease in AP-1 DNA binding activity was seen in response to both inducing stimuli. This decrease in AP-1 binding activity may be mediated by an increase in the activity of an AP-1 inhibitory factor, as the steady state levels of jun protein remained constant during the onset of apoptosis, and cytosolic AP-1 inhibitory activity was found to increase, concomitant with the decrease in AP-1 DNA binding activity. Our data demonstrate the complexity of the mechanisms involved in the regulation of c-jun expression during the onset of apoptosis, and suggest a novel mode for the regulation of AP-1 activity during the cessation of proliferation.
c-jun基因的产物是转录因子AP-1的一个组成部分,AP-1在细胞对某些增殖刺激的反应中起关键的调节作用。在本报告中,我们证明了在用地塞米松或γ射线处理人白血病T细胞系CEM C7诱导凋亡过程中,c-jun mRNA的表达持续延长。然而,c-jun mRNA的过表达并未伴随着jun蛋白表达的增加或AP-1 DNA结合活性的增强。实际上,在两种诱导刺激下均观察到AP-1 DNA结合活性降低。AP-1结合活性的这种降低可能是由AP-1抑制因子活性增加介导的,因为在凋亡开始时jun蛋白的稳态水平保持恒定,并且发现胞质AP-1抑制活性增加,与AP-1 DNA结合活性降低同时出现。我们的数据证明了凋亡开始期间c-jun表达调控机制的复杂性,并提示了增殖停止期间AP-1活性调控的一种新模式。