Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.
Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.
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G1/S 转变期间 miR-17-92 簇调控的癌症网络的稳健性和主干基序
DOI：
10.1371/journal.pone.0057009
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Jia Y
中科院分区：
文献类型：
--
作者：
Yang L;Meng Y;Bao C;Liu W;Ma C;Li A;Xuan Z;Shan G;Jia Y
基于转录因子、癌基因、肿瘤抑制因子和microRNA之间的相互作用，构建了一个miR-17-92簇调控的肿瘤网络布尔模型，该网络与哺乳动物细胞周期G1/S转换的调控有关。利用布尔网络理论研究了该调节网络的鲁棒性。研究发现，在细胞周期的G1/S转换过程中，调控网络是鲁棒的，并且对于小的扰动，网络的鲁棒性在很大程度上得以保持.通过使用独特的基于过程的方法，该网络的结构进行了分析。它表明，该网络可以分解成一个骨干基序，提供了主要的生物功能，和一个剩余的基序，使调节系统更稳定。我们的模型显示了miR-17-92在抑制G1/S细胞周期检查点和通过靶向相互作用蛋白的遗传网络增加癌细胞不受控制的增殖中的关键作用。
Based on interactions among transcription factors, oncogenes, tumor suppressors and microRNAs, a Boolean model of cancer network regulated by miR-17-92 cluster is constructed, and the network is associated with the control of G1/S transition in the mammalian cell cycle. The robustness properties of this regulatory network are investigated by virtue of the Boolean network theory. It is found that, during G1/S transition in the cell cycle process, the regulatory networks are robustly constructed, and the robustness property is largely preserved with respect to small perturbations to the network. By using the unique process-based approach, the structure of this network is analyzed. It is shown that the network can be decomposed into a backbone motif which provides the main biological functions, and a remaining motif which makes the regulatory system more stable. The critical role of miR-17-92 in suppressing the G1/S cell cycle checkpoint and increasing the uncontrolled proliferation of the cancer cells by targeting a genetic network of interacting proteins is displayed with our model.
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