Elucidating the interactions between the adhesive and transcriptional functions of -catenin in normal and cancerous cells
Open accessAbstract
Wnt signalling is involved in a wide range of physiological and pathological processes. The presence of an extracellular Wnt stimulus induces cytoplasmic stabilisation and nuclear translocation of beta-catenin, a protein that also plays an essential role in cadherin-mediated adhesion. Two main hypotheses have been proposed concerning the balance between beta-catenin's adhesive and transcriptional functions: either beta-catenin's fate is determined by competition between its binding partners, or Wnt induces folding of beta-catenin into a conformation allocated preferentially to transcription. The experimental data supporting each hypotheses remain inconclusive. In this paper we present a new mathematical model of the Wnt pathway that incorporates beta-catenin's dual function. We use this model to carry out a series of in silico experiments and compare the behaviour of systems governed by each hypothesis. Our analytical results and model simulations provide further insight into the current understanding of Wnt signalling and, in particular, reveal differences in the response of the two modes of interaction between adhesion and signalling in certain in silico settings. We also exploit our model to investigate the impact of the mutations most commonly observed in human colorectal cancer. Simulations show that the amount of functional APC required to maintain a normal phenotype increases with increasing strength of the Wnt signal, a result which illustrates that the environment can substantially influence both tumour initiation and phenotype.
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The simulation models developed in [29, 32, 34-36, 39, 41] had neither been calibrated nor validated explicitly, because they used parameter values from other studies.
“The simulations models developed in [29, 32, 34–36, 39, 41] had neither been calibrated nor validated explicitly, because they used parameter values from other studies.”
From Relating simulation studies by provenance—Developing a family of Wnt signaling models (2021) · cites this paper as [34]
All other simulation studies either used wet-lab data from other publications or did not explicitly refer to wet-lab data at all [29, 30, 33, 34, 39, 41, 53].
“All other simulation studies either used wet-lab data from other publications or did not explicitly refer to wet-lab data at all [29, 30, 33, 34, 39, 41, 53].”
From Relating simulation studies by provenance—Developing a family of Wnt signaling models (2021) · cites this paper as [34]
Some studies develop a story line where a simulation model has been successively refined, extended, or composed ([28, 33, 34, 36, 41, 46, 48, 49, 51, 56]).
“Some studies develop a story line where a simulation model has been successively refined, extended, or composed ([28, 33, 34, 36, 41, 46, 48, 49, 51, 56]).”
From Relating simulation studies by provenance—Developing a family of Wnt signaling models (2021) · cites this paper as [34]
The central cluster includes the Wnt model by Lee et al. (2003) as well as the studies [30, 34, 35, 41].
“The central cluster includes the Wnt model by Lee et al. (2003) [28] as well as the studies [30, 34, 35, 41].”
From Relating simulation studies by provenance—Developing a family of Wnt signaling models (2021) · cites this paper as [34]
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- Authors
- van Leeuwen, I. M. M., Byrne, H. M., Jensen, O. E., & King, J. R.
- Affiliations
- University of Nottingham (GB)
- Venue
- Journal of Theoretical Biology
- Publisher
- Elsevier BV
- Published
- 2007-07
- Volume
- 247
- Issue
- 1
- Pages
- 77-102
- ISSN
- 0022-5193 (ISSN-L)
- OpenAlex
- W2006006356
- Cited by
- 59
- References
- 126
- Citations by year
- 2026: 1 · 2025: 1 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 5 · 2017: 3 · 2016: 2 · 2015: 5 · 2014: 4 · 2013: 5 · 2012: 6
- FWCI
- 2.12
- Type
- journal article
- Language
- en
- Open access
- Licence
- Locations
- Journal of Theoretical Biology (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Repository@Nottingham (University of Nottingham) (submittedVersion, cc-by)
- Repository@Nottingham (University of Nottingham) (submittedVersion, other-oa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Physical Sciences › Mathematics › Modeling and Simulation › Mathematical Biology Tumor Growth
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gene Regulatory Network Analysis
- Keywords
- β-catenin, Wnt signaling, cadherin-mediated adhesion, transcriptional regulation, APC mutation, colorectal cancer, tumor initiation, nuclear translocation, protein folding, computer simulation
- MeSH terms
- Cell Adhesion, Cell Transformation, Neoplastic, Humans, Models, Biological, Mutation, Neoplasm Proteins, Transcription, Genetic, Colorectal Neoplasms, Signal Transduction, Cadherins, Genes, APC, Wnt Proteins, beta Catenin
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