Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.

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...

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Main Authors: Lijian Yang, Yan Meng, Chun Bao, Wangheng Liu, Chengzhang Ma, Anbang Li, Zhan Xuan, Ge Shan, Ya Jia
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3585929?pdf=render
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spelling doaj-003e606d1f4d43768b05f5f46345df1c2020-11-25T02:19:47ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0183e5700910.1371/journal.pone.0057009Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.Lijian YangYan MengChun BaoWangheng LiuChengzhang MaAnbang LiZhan XuanGe ShanYa JiaBased 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.http://europepmc.org/articles/PMC3585929?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Lijian Yang
Yan Meng
Chun Bao
Wangheng Liu
Chengzhang Ma
Anbang Li
Zhan Xuan
Ge Shan
Ya Jia
spellingShingle Lijian Yang
Yan Meng
Chun Bao
Wangheng Liu
Chengzhang Ma
Anbang Li
Zhan Xuan
Ge Shan
Ya Jia
Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.
PLoS ONE
author_facet Lijian Yang
Yan Meng
Chun Bao
Wangheng Liu
Chengzhang Ma
Anbang Li
Zhan Xuan
Ge Shan
Ya Jia
author_sort Lijian Yang
title Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.
title_short Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.
title_full Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.
title_fullStr Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.
title_full_unstemmed Robustness and backbone motif of a cancer network regulated by miR-17-92 cluster during the G1/S transition.
title_sort robustness and backbone motif of a cancer network regulated by mir-17-92 cluster during the g1/s transition.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2013-01-01
description 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.
url http://europepmc.org/articles/PMC3585929?pdf=render
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