The overshoot and phenotypic equilibrium in characterizing cancer dynamics of reversible phenotypic plasticity

DOI10.1016/J.JTBI.2015.11.008zbMATH Open1343.92212arXiv1503.04558OpenAlexW1792459243WikidataQ50763018 ScholiaQ50763018MaRDI QIDQ304808FDOQ304808

Authors: Xiufang Chen, Tianquan Feng, Ming Yi, Da Zhou, Xing'an Zhang, Yue Wang 

Publication date: 26 August 2016

Published in: Journal of Theoretical Biology (Search for Journal in Brave)

Abstract: The paradigm of phenotypic plasticity indicates reversible relations of different cancer cell phenotypes, which extends the cellular hierarchy proposed by the classical cancer stem cell (CSC) theory. Since it is still question able if the phenotypic plasticity is a crucial improvement to the hierarchical model or just a minor extension to it, it is worthwhile to explore the dynamic behavior characterizing the reversible phenotypic plasticity. In this study we compare the hierarchical model and the reversible model in predicting the cell-state dynamics observed in biological experiments. Our results show that the hierarchical model shows significant disadvantages over the reversible model in describing both long-term stability (phenotypic equilibrium) and short-term transient dynamics (overshoot) of cancer cells. In a very specific case in which the total growth of population due to each cell type is identical, the hierarchical model predicts neither phenotypic equilibrium nor overshoot, whereas thereversible model succeeds in predicting both of them. Even though the performance of the hierarchical model can be improved by relaxing the specific assumption, its prediction to the phenotypic equilibrium strongly depends on a precondition that may be unrealistic in biological experiments, and it also fails to capture the overshoot of CSCs. By comparison, it is more likely for the reversible model to correctly describe the stability of the phenotypic mixture and various types of overshoot behavior.

Full work available at URL: https://arxiv.org/abs/1503.04558

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zbMATH Keywords

cancer stem cell modelcell plasticitymulti-phenotypic modeltransient dynamics

Mathematics Subject Classification ID

Medical applications (general) (92C50) Genetics and epigenetics (92D10) Cell biology (92C37)

Cites Work

• A multicompartment mathematical model of cancer stem cell-driven tumor growth dynamics
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Cited In (6)

• On tumoural growth and treatment under cellular dedifferentiation
• Inference on autoregulation in gene expression with variance-to-mean ratio
• The phenotypic equilibrium of cancer cells: from average-level stability to path-wise convergence
• Replicator dynamics of cancer stem cell: selection in the presence of differentiation and plasticity
• Cell population growth kinetics in the presence of stochastic heterogeneity of cell phenotype
• A Bayesian statistical analysis of stochastic phenotypic plasticity model of cancer cells

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