ArticleNPJ systems biology and applications2024
A Boolean model explains phenotypic plasticity changes underlying hepatic cancer stem cells emergence.
Article in NPJ systems biology and applications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- In silico models in oncology, neurology, and epidemiology: systems-level and multiscale perspectives.NPJ systems biology and applications · 2026Review
- Path-based quantification of activation and repression in Boolean models using BooLEVARD.NPJ systems biology and applications · 2025Article
- Analytical approach of synchronous and asynchronous update schemes applied to solving biological Boolean networks.PloS one · 2025Article
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4 authors.
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Abstract
In several carcinomas, including hepatocellular carcinoma, it has been demonstrated that cancer stem cells (CSCs) have enhanced invasiveness and therapy resistance compared to differentiated cancer cells. Mathematical-computational tools could be valuable for integrating experimental results and understanding the phenotypic plasticity mechanisms for CSCs emergence. Based on the literature review, we constructed a Boolean model that recovers eight stable states (attractors) corresponding to the gene expression profile of hepatocytes and mesenchymal cells in senescent, quiescent, proliferative, and stem-like states. The epigenetic landscape associated with the regulatory network was analyzed. We observed that the loss of p53, p16, RB, or the constitutive activation of β-catenin and YAP1 increases the robustness of the proliferative stem-like phenotypes. Additionally, we found that p53 inactivation facilitates the transition of proliferative hepatocytes into stem-like mesenchymal phenotype. Thus, phenotypic plasticity may be altered, and stem-like phenotypes related to CSCs may be easier to attain following the mutation acquisition.
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