University at Buffalo, The State University of New York, Buffalo, NY
"A Computational Model of Metastatic Cancer Cell Migration Phenotype: Single and Collective Migration"
Metastasis is a complex process that involves the spread of cancer cells from the primary tumor location to distant organs. During metastasis, cancer cells acquire migratory phenotypes, which allow them to detach from the primary tumor and invade the surrounding tissue. Cancer cells migrate through various mechanisms in the tumor microenvironment (TME), including single and collective migration phenotypes. These migration phenotypes are regulated by a complex interplay between the TME, particularly the extracellular matrix (ECM), and the signaling pathways. Here, we developed a computational model using open-source software CompuCell3D (a cellular Potts lattice-based model) that mimics in vitro migration studies of single and collective migration. We consider cancer cells as discrete agents, and their interactions with the TME are simulated in Compucell3D. Using the model, we analyzed the effect of cell-cell adhesion force, non-invasive and invasive phenotypes and structures, and cell-TME interactions in single and collective cell migration. Our aim is to identify key parameters and regulators of cancer metastasis and migration phenotypes. Our model will provide a better understanding of the underlying mechanisms essential for developing more targeted and personalized therapies for cancer metastasis.
Additional authors: Ashlee N. Ford Versypt; Department of Chemical and Biological Engineering, University at Buffalo, The State University of New York, Buffalo, NY