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System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia

BACKGROUND: Molecular mechanisms of the functional alteration of hematopoietic stem cells (HSCs) in leukemic environment attract intensive research interests. As known in previous researches, Maff and Egr3 are two important genes having opposite functions on cell cycle; however, they are both highly...

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Autores principales: Li, Rudong, Wang, Yin, Cheng, Hui, Liu, Gang, Cheng, Tao, Liu, Yunlong, Liu, Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5629552/
https://www.ncbi.nlm.nih.gov/pubmed/28984203
http://dx.doi.org/10.1186/s12918-017-0467-4
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author Li, Rudong
Wang, Yin
Cheng, Hui
Liu, Gang
Cheng, Tao
Liu, Yunlong
Liu, Lei
author_facet Li, Rudong
Wang, Yin
Cheng, Hui
Liu, Gang
Cheng, Tao
Liu, Yunlong
Liu, Lei
author_sort Li, Rudong
collection PubMed
description BACKGROUND: Molecular mechanisms of the functional alteration of hematopoietic stem cells (HSCs) in leukemic environment attract intensive research interests. As known in previous researches, Maff and Egr3 are two important genes having opposite functions on cell cycle; however, they are both highly expressed in HSCs under leukemia. Hence, exploring the molecular mechanisms of how the genes act on cell cycle will help revealing the functional alteration of HSCs. RESULTS: We herein utilize the bioinformatic resources to computationally model the acting mechanisms of Maff and Egr3 on cell cycle. Using the data of functional experiments as reference, molecular acting mechanisms are optimally enumerated through model selection. The results are consolidated by evidences from gene sequence analysis, thus having enhanced the confidence of our pilot findings, which suggest that HSCs possibly undergo a “adaptation - suppression” process in response to the malignant environment of leukemia. CONCLUSION: As a pilot research, our results may provide valuable insights for further experimental studies. Meanwhile, our research method combining computational modeling and data from functional experiments can be worthwhile for knowledge discovery; and it can be generalized and extended to other biological/biomedical studies. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12918-017-0467-4) contains supplementary material, which is available to authorized users.
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spelling pubmed-56295522017-10-13 System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia Li, Rudong Wang, Yin Cheng, Hui Liu, Gang Cheng, Tao Liu, Yunlong Liu, Lei BMC Syst Biol Research BACKGROUND: Molecular mechanisms of the functional alteration of hematopoietic stem cells (HSCs) in leukemic environment attract intensive research interests. As known in previous researches, Maff and Egr3 are two important genes having opposite functions on cell cycle; however, they are both highly expressed in HSCs under leukemia. Hence, exploring the molecular mechanisms of how the genes act on cell cycle will help revealing the functional alteration of HSCs. RESULTS: We herein utilize the bioinformatic resources to computationally model the acting mechanisms of Maff and Egr3 on cell cycle. Using the data of functional experiments as reference, molecular acting mechanisms are optimally enumerated through model selection. The results are consolidated by evidences from gene sequence analysis, thus having enhanced the confidence of our pilot findings, which suggest that HSCs possibly undergo a “adaptation - suppression” process in response to the malignant environment of leukemia. CONCLUSION: As a pilot research, our results may provide valuable insights for further experimental studies. Meanwhile, our research method combining computational modeling and data from functional experiments can be worthwhile for knowledge discovery; and it can be generalized and extended to other biological/biomedical studies. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12918-017-0467-4) contains supplementary material, which is available to authorized users. BioMed Central 2017-10-03 /pmc/articles/PMC5629552/ /pubmed/28984203 http://dx.doi.org/10.1186/s12918-017-0467-4 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Li, Rudong
Wang, Yin
Cheng, Hui
Liu, Gang
Cheng, Tao
Liu, Yunlong
Liu, Lei
System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia
title System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia
title_full System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia
title_fullStr System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia
title_full_unstemmed System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia
title_short System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia
title_sort system modeling reveals the molecular mechanisms of hsc cell cycle alteration mediated by maff and egr3 under leukemia
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5629552/
https://www.ncbi.nlm.nih.gov/pubmed/28984203
http://dx.doi.org/10.1186/s12918-017-0467-4
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