Researchers from GNS, UCSD, and HHMI used a combined experimental and computational approach to understand the progression of the mammalian G1 cell cycle.
Researchers reported results describing a missing link between metabolic pathways and cell reproduction, which they believe could become a new target that will halt cancer-cell replication and tumor growth.
The study, “A Systems Biology Dynamical Model of Mammalian G1 Cell Cycle Progression”, was published in Molecular Systems Biology. It was co-authored by researchers at Gene Network Sciences (GNS), the Howard Hughes Medical Institute (HHMI), and Department of Cellular and Molecular Medicine at the University of California San Diego (UCSD).
The paper describes a combined experimental and computational approach used to understand progression of the mammalian G1 cell cycle, one of the phases in mammalian cell reproduction and tumor growth.
“This is the first time that quantitative evidence has pointed to the necessary existence of a key metabolic factor controlling passage through the restriction point in the cell cycle that commits the cell to DNA replication,” notes Steve Dowdy, Ph.D., the principal UCSD investigator and HHMI researcher. “The combined efforts of our lab and the GNS team and their software has allowed us to probe further into the inner workings of cell replication and the origins of cancerous cell growth.”
The scientists used GNS software to create a quantitative computer model that accurately simulates G1 cell cycle progression and was able to reproduce observations from in vitro cell culture studies. Specifically, they used the quantitative reverse-engineering and modeling approach to predict the presence of a previously unidentified modifier that is postulated to cause transition of the cell cycle from the growth-factor dependent early G1 phase to the growth-factor independent late G1 phase.