ArticleInterface focus2014
The balance between cell cycle arrest and cell proliferation: control by the extracellular matrix and by contact inhibition.
Article in Interface focus, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
86 citing papers in PubMed, 195 citations in OpenAlex.
- Effect of food on the pharmacokinetics of the WEE1 inhibitor adavosertib (AZD1775) in patients with advanced solid tumors.Cancer chemotherapy and pharmacology · 2020Trial
- Passive nuclear transport deviates from Fickian behavior in prostate and breast cell types.Nucleus (Austin, Tex.) · 2026Article
- The Roles of myomiRs in the Pathogenesis of Sarcopenia: From Literature to In Silico Analysis.Molecular biotechnology · 2026Review
- Extracellular matrix-derived mechanical force induces CDK4/6 inhibitor resistance by inhibiting NEK10 dependent cell cycle regulation in breast cancer.International journal of surgery (London, England) · 2026Article
- Cell Population Dynamics Informed by Cell-Cycle Regulation: A Deterministic Modeling Toolkit.Computational and structural biotechnology journal · 2026Review
- Effect of Extracellular Matrix Derived from Porcine Tissue on Stemness of Porcine Spermatogonial Stem Cells.International journal of molecular sciences · 2025Article
- Femtosecond Laser-Engineered β-TCP Scaffolds: A Comparative Study of Green-Synthesized AgNPs vs. Ion Doping AgainstInternational journal of molecular sciences · 2025Article
- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
- Comprehensive analysis of cellular metrics: From proliferation to mitochondrial membrane potential and cell death in a single sample.Cell death discovery · 2025Article
- Open-Label, Multicenter, Phase I Study to Assess Safety and Tolerability of Adavosertib Plus Durvalumab in Patients with Advanced Solid Tumors.Targeted oncology · 2025Article
- Adavosertib in Combination with Olaparib in Patients with Refractory Solid Tumors: An Open-Label, Dose-Finding, and Dose-Expansion Phase Ib Trial.Targeted oncology · 2024Article
- Dual-Function Femtosecond Laser: β-TCP Structuring and AgNP Synthesis via Photoreduction with Azorean Green Tea for Enhanced Osteointegration and Antibacterial Properties.Materials (Basel, Switzerland) · 2024Article
- A comprehensive review of computational cell cycle models in guiding cancer treatment strategies.NPJ systems biology and applications · 2024Review
- Finding a Direct Method for a Dynamic Process: The DD (Direct and Dynamic) Cell-Tox Method.International journal of molecular sciences · 2024Article
- Excavatolide C/cisplatin combination induces antiproliferation and drives apoptosis and DNA damage in bladder cancer cells.Archives of toxicology · 2024Article
- Tension-induced adhesion mode switching: the interplay between focal adhesions and clathrin-containing adhesion complexes.bioRxiv : the preprint server for biology · 2024Article
- Heme Oxygenase-1 and Its Role in Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- The effect of serum origin on cytokines induced killer cell expansion and function.BMC immunology · 2023Article
- Article
- A Phase Ib Study Assessing the Safety, Tolerability, and Efficacy of the First-in-Class Wee1 Inhibitor Adavosertib (AZD1775) as Monotherapy in Patients with Advanced Solid Tumors.Targeted oncology · 2023Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To understand the dynamics of the cell cycle, we need to characterize the balance between cell cycle arrest and cell proliferation, which is often deregulated in cancers. We address this issue by means of a detailed computational model for the network of cyclin-dependent kinases (Cdks) driving the mammalian cell cycle. Previous analysis of the model focused on how this balance is controlled by growth factors (GFs) or the levels of activators (oncogenes) and inhibitors (tumour suppressors) of cell cycle progression. Supra-threshold changes in the level of any of these factors can trigger a switch in the dynamical behaviour of the Cdk network corresponding to a bifurcation between a stable steady state, associated with cell cycle arrest, and sustained oscillations of the various cyclin/Cdk complexes, corresponding to cell proliferation. Here, we focus on the regulation of cell proliferation by cellular environmental factors external to the Cdk network, such as the extracellular matrix (ECM), and contact inhibition, which increases with cell density. We extend the model for the Cdk network by including the phenomenological effect of both the ECM, which controls the activation of the focal adhesion kinase (FAK) that promotes cell cycle progression, and cell density, which inhibits cell proliferation via the Hippo/YAP pathway. The model shows that GFs and FAK activation are capable of triggering in a similar dynamical manner the transition to cell proliferation, while the Hippo/YAP pathway can arrest proliferation once cell density passes a critical threshold. The results account for the dependence or independence of cell proliferation on serum and/or cell anchorage to ECM. Whether the balance in the Cdk network is tilted towards cell cycle arrest or proliferation depends on the direction in which the threshold associated with the bifurcation is passed once the cell integrates the multiple, internal or external signals that promote or impede progression in the cell cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.