ArticleComputational and mathematical methods in medicine2016
A Computational Model for Investigating Tumor Apoptosis Induced by Mesenchymal Stem Cell-Derived Secretome.
Article in Computational and mathematical methods in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Review
- Mechanistic characterization of endothelial sprouting mediated by pro-angiogenic signaling.Microcirculation (New York, N.Y. : 1994) · 2022Article
- Systems Biology to Understand and Regulate Human Retroviral Proinflammatory Response.Frontiers in immunology · 2021Review
- Multiscale modeling of tumor response to vascular endothelial growth factor (VEGF) inhibitor.In silico biology · 2021Article
- Article
- Data-driven analysis of a mechanistic model of CAR T cell signaling predicts effects of cell-to-cell heterogeneity.Journal of theoretical biology · 2020Article
- A hybrid multiscale model for investigating tumor angiogenesis and its response to cell-based therapy.In silico biology · 2019Review
- Mechanistic insight into activation of MAPK signaling by pro-angiogenic factors.BMC systems biology · 2018Article
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Authors and funding
2 authors.
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Abstract
Apoptosis is a programmed cell death that occurs naturally in physiological and pathological conditions. Defective apoptosis can trigger the development and progression of cancer. Experiments suggest the ability of secretome derived from mesenchymal stem cells (MSC) to induce apoptosis in cancer cells. We develop a hybrid discrete-continuous multiscale model to further investigate the effect of MSC-derived secretome in tumor growth. The model encompasses three biological scales. At the molecular scale, a system of ordinary differential equations regulate the expression of proteins involved in apoptosis signaling pathways. At the cellular scale, discrete equations control cellular migration, phenotypic switching, and proliferation. At the extracellular scale, a system of partial differential equations are employed to describe the dynamics of microenvironmental chemicals concentrations. The simulation is able to produce both avascular tumor growth rate and phenotypic patterns as observed in the experiments. In addition, we obtain good quantitative agreements with the experimental data on the apoptosis of HeLa cancer cells treated with MSC-derived secretome. We use this model to predict the growth of avascular tumor under various secretome concentrations over time.
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