Br-cAMP induction of apoptosis in synchronized CHO cells.

L R Gurley, A L Jandacek, J G Valdez, R J Sebring, J A D'Anna, T T Puck
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引用次数: 7

Abstract

The proliferation of suspension cultures of malignant CHO cells was inhibited by 0.5 mM Br-cAMP treatment and restored by its removal. This treatment also inhibited histone H1 phosphorylation completely, reduced histones H2A and H4 phosphorylations, induced DNA degradation, and produced cells containing micronuclei. Agarose gel electrophoresis of the degraded DNA fragments produced a "ladder" pattern confirming these cells were undergoing apoptosis. Cell cycle synchrony experiments demonstrated culture growth inhibition was the result of two different cell cycle-specific processes: [1] arrested cell cycle traverse at a restriction point in mid-G1, and [2] rapid apoptosis following cell division. Br-cAMP did not stop cells in late-G1, S, G2, or M from traversing the cell cycle and dividing, but rather, induced apoptosis following mitosis. The restriction point of Br-cAMP arrest was located in the middle of a wider band of G1 arrest induced by isoleucine deprivation. The cells synchronized in G1 before the restriction point were held in G1-arrest by Br-cAMP and spared apoptotic death. These studies support the further study of cAMP derivatives as agents to induce tumor regression by apoptosis and reverse transformation.

Br-cAMP诱导同步CHO细胞凋亡。
0.5 mM Br-cAMP可抑制恶性CHO细胞悬浮培养的增殖,去除后细胞增殖恢复。该处理还完全抑制组蛋白H1磷酸化,降低组蛋白H2A和H4磷酸化,诱导DNA降解,并产生含有微核的细胞。琼脂糖凝胶电泳降解的DNA片段产生“阶梯”模式,证实这些细胞正在发生凋亡。细胞周期同步实验表明,培养生长抑制是两个不同的细胞周期特异性过程的结果:[1]在g1中期的一个限制点阻止细胞周期穿越,[2]细胞分裂后快速凋亡。Br-cAMP不能阻止g1、S、G2或M晚期的细胞穿越细胞周期和分裂,而是诱导有丝分裂后的细胞凋亡。Br-cAMP阻滞的限制点位于异亮氨酸剥夺引起的G1阻滞更宽频带的中间。在限制点前同步于G1的细胞被Br-cAMP保持在G1阻滞状态,免于凋亡死亡。这些研究为进一步研究cAMP衍生物通过细胞凋亡和逆转转化诱导肿瘤消退提供了依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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