ArticlePharmaceutical research2019
A Theoretical Model for the Cell Cycle and Drug Induced Cell Cycle Arrest of FUCCI Systems with Cell-to-Cell Variation during Mitosis.
Article in Pharmaceutical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Mezigdomide combined with bortezomib disrupts the cell cycle and elicits superior antitumor effects in multiple myeloma.Blood neoplasia · 2026Article
- Tumor-infiltrating bacteria disrupt cancer epithelial cell interactions and induce cell-cycle arrest.Cancer cell · 2026Article
- Folate-based binuclear Mn(II) chelates with 2,2'-bipyridine/1,10-phenanthroline as targeted anticancer agents for colon cancer cells.Scientific reports · 2025Article
- Interdependency of estradiol-mediated ERα activation and subsequent PR and GREB1 induction to control cell cycle progression.Heliyon · 2024Article
- A comprehensive review of computational cell cycle models in guiding cancer treatment strategies.NPJ systems biology and applications · 2024Review
- Merits and Demerits of ODE Modeling of Physicochemical Systems for Numerical Simulations.Molecules (Basel, Switzerland) · 2022Review
- Mathematical models incorporating a multi-stage cell cycle replicate normally-hidden inherent synchronization in cell proliferation.Journal of the Royal Society, Interface · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
purposeSince the molecular mechanism of the cell cycle was established, various theoretical models of this process have been developed. A recent study revealed significant variability in cell cycle duration between mother and daughter cells, but this observation has not been incorporated into the theoretical models.
methodsWe used fluorescent ubiquitination-based cell cycle indicator (FUCCI) systems and live-monitored the heterogeneity of cell cycle progression within daughter cells, which accounts for dephasing synchrony. To incorporate the variable cell cycle durations into a model, we modified a two-ordinary differential equation (ODE) model based on reciprocal activation between CDK1 and APC.
resultsOur model reproduced the experimental population profile, in which cell cycle synchrony dephased due to variability. Based on this model, we determined parameters for CDK1 and APC in the cell cycle profile after treatment with antimitotic drugs and associated the parameters with the drugs' mode of action as cell cycle inhibitors.
conclusionThis suggests that this model is useful for determining the mode of action of unknown small molecules on the cell cycle.
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