System modeling reveals the molecular mechanisms of HSC cell cycle alteration mediated by Maff and Egr3 under leukemia
Year: 2017
Type: article
Abstract: 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.
Source: BMC Systems Biology
Authors: Rudong Li, Yin Wang, Hui Cheng, Gang Liu, Tao Cheng, Yunlong Liu, Lei Liu
Institutions: Indiana University Indianapolis, Indiana University School of Medicine, Shanghai Medical College of Fudan University, Fudan University, Shanghai Public Health Clinical Center, Shanghai Center For Bioinformation Technology, Chinese Academy of Medical Sciences & Peking Union Medical College
Language: English
Subfield: Hematology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,290
OpenAlex ID: W2762353132
