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首页> 外文期刊>Cell cycle >ARTD1 regulates cyclin E expression and consequently cell-cycle re-entry and G(1)/S progression in T24 bladder carcinoma cells
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ARTD1 regulates cyclin E expression and consequently cell-cycle re-entry and G(1)/S progression in T24 bladder carcinoma cells

机译：ARTD1调节细胞周期蛋白E的表达，从而调节T24膀胱癌细胞的细胞周期再进入和G（1）/ S进程

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摘要

ADP-ribosylation is involved in a variety of biological processes, many of which are chromatin-dependent and linked to important functions during the cell cycle. However, any study on ADP-ribosylation and the cell cycle faces the problem that synchronization with chemical agents or by serum starvation and subsequent growth factor addition already activates ADP-ribosylation by itself. Here, we investigated the functional contribution of ARTD1 in cell cycle re-entry and G(1)/S cell cycle progression using T24 urinary bladder carcinoma cells, which synchronously re-enter the cell cycle after splitting without any additional stimuli. In synchronized cells, ARTD1 knockdown, but not inhibition of its enzymatic activity, caused specific down-regulation of cyclin E during cell cycle re-entry and G(1)/S progression through alterations of the chromatin composition and histone acetylation, but not of other E2F-1 target genes. Although Cdk2 formed a functional complex with the residual cyclin E, p27(Kip1) protein levels increased in G(1) upon ARTD1 knockdown most likely due to inappropriate cyclin E-Cdk2-induced phosphorylation-dependent degradation, leading to decelerated G(1)/S progression. These results provide evidence that ARTD1 regulates cell cycle re-entry and G(1)/S progression via cyclin E expression and p27(Kip1) stability independently of its enzymatic activity, uncovering a novel cell cycle regulatory mechanism.
机译：ADP-核糖基化涉及多种生物学过程，其中许多是染色质依赖性的，并在细胞周期中与重要功能相关。然而，任何有关ADP-核糖基化和细胞周期的研究都面临着与化学试剂同步或通过血清饥饿和随后的生长因子添加本身已经激活ADP-核糖基化的问题。在这里，我们研究了ARTD1在使用T24膀胱癌细胞的细胞周期再进入和G（1）/ S细胞周期进展中的功能性贡献，它们在分裂后同步地重新进入细胞周期而没有任何其他刺激。在同步细胞中，ARTD1敲低但未抑制其酶促活性，导致细胞周期重新进入和细胞周期蛋白E的特异性下调，以及通过染色质组成和组蛋白乙酰化的改变而引起的G（1）/ S进程，但不是其他E2F-1靶基因。虽然Cdk2与残留的细胞周期蛋白E形成功能复合物，但ARTD1敲低后，G（1）中的p27（Kip1）蛋白水平增加，最可能是由于不适当的细胞周期蛋白E-Cdk2诱导的磷酸化依赖性降解，导致G（1）减速。 / S进度。这些结果提供了证据，表明ARTD1通过细胞周期蛋白E表达和p27（Kip1）稳定性独立于其酶促活性来调节细胞周期的再进入和G（1）/ S进程，揭示了一种新型的细胞周期调节机制。

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