ArticleFrontiers in oncology2013
Mathematical modeling of cancer invasion: the role of membrane-bound matrix metalloproteinases.
Article in Frontiers in oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 53 citations in OpenAlex.
- Multiscale Modelling, Analysis and Simulation of Cancer Invasion Mediated by Bound and Soluble Enzymes.Bulletin of mathematical biology · 2025Article
- Modelling the Impact of HIF on Metabolism and the Extracellular Matrix: Consequences for Tumour Growth and Invasion.Bulletin of mathematical biology · 2025Article
- Modelling the Effect of Matrix Metalloproteinases in Dermal Wound Healing.Bulletin of mathematical biology · 2023Article
- A multi-layered hybrid model for cancer cell invasion.Medical & biological engineering & computing · 2022Article
- Directionality of Macrophages Movement in Tumour Invasion: A Multiscale Moving-Boundary Approach.Bulletin of mathematical biology · 2020Article
- Cell-Scale Degradation of Peritumoural Extracellular Matrix Fibre Network and Its Role Within Tissue-Scale Cancer Invasion.Bulletin of mathematical biology · 2020Article
- A Mathematical Framework for Modelling the Metastatic Spread of Cancer.Bulletin of mathematical biology · 2019Article
- Brucine suppresses breast cancer metastasis via inhibiting epithelial mesenchymal transition and matrix metalloproteinases expressions.Chinese journal of integrative medicine · 2018Article
- Structured models of cell migration incorporating molecular binding processes.Journal of mathematical biology · 2017Article
- miR-1908 as a novel prognosis marker of glioma via promoting malignant phenotype and modulating SPRY4/RAF1 axis.Oncology reports · 2017Article
- A biochemo-mechano coupled, computational model combining membrane transport and pericellular proteolysis in tissue mechanics.Proceedings. Mathematical, physical, and engineering sciences · 2017Article
- miR-125b-5p functions as a tumor suppressor gene partially by regulating HMGA2 in esophageal squamous cell carcinoma.PloS one · 2017Article
- Cell Invasion Dynamics into a Three Dimensional Extracellular Matrix Fibre Network.PLoS computational biology · 2015Article
- An engineered TIMP2-based and enediyne-integrated fusion protein for targeting MMP-14 shows potent antitumor efficacy.Oncotarget · 2015Article
- Expression levels of seprase/FAPα and DPPIV/CD26 in epithelial ovarian carcinoma.Oncology letters · 2015Article
- Nimbolide inhibits invasion and migration, and down-regulates uPAR chemokine gene expression, in two breast cancer cell lines.Cell proliferation · 2014Article
- Article
- Simulating cancer: computational models in oncology.Frontiers in oncology · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the hallmarks of cancer growth and metastatic spread is the process of local invasion of the surrounding tissue. Cancer cells achieve protease-dependent invasion by the secretion of enzymes involved in proteolysis. These overly expressed proteolytic enzymes then proceed to degrade the host tissue allowing the cancer cells to disseminate throughout the microenvironment by active migration and interaction with components of the extracellular matrix (ECM) such as collagen. In this paper we develop a mathematical model of cancer invasion which consider the role of matrix metalloproteinases (MMPs). Specifically our model will focus on two distinct types of MMP, i.e., soluble, diffusible MMPs (e.g., MMP-2) and membrane-bound MMPs (e.g., MT1-MMP), and the roles each of these plays in cancer invasion. The implications of MMP-2 activation by MMP-14 and the tissue inhibitor of metalloproteinases-2 are considered alongside the effect the architecture of the matrix may have when applied to a model of cancer invasion. Elements of the ECM architecture investigated include pore size of the matrix, since in some highly dense collagen structures such as breast tissue, the cancer cells are unable to physically fit through a porous region, and the crosslinking of collagen fibers. In this scenario, cancer cells rely on membrane-bound MMPs to forge a path through which degradation by other MMPs and movement of cancer cells becomes possible.
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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.