Abstract
Tumor cells migrate through changing microenvironments of diseased and healthy tissue, making their migration particularly challenging to describe. To better understand this process, computational models have been developed for both the ameboid and mesenchymal modes of cell migration. Here, we review various approaches that have been used to account for the physical environment's effect on cell migration in computational models, with a focus on their application to understanding cancer metastasis and the related phenomenon of durotaxis. We then discuss how mesenchymal migration models typically simulate complex cell–extracellular matrix (ECM) interactions, while ameboid migration models use a cell-focused approach that largely ignores ECM when not acting as a physical barrier. This approach greatly simplifies or ignores the mechanosensing ability of ameboid migrating cells and should be reevaluated in future models. We conclude by describing future model elements that have not been included to date but would enhance model accuracy.
Highlights
We discuss how mesenchymal migration models typically simulate complex cell–extracellular matrix (ECM) interactions, while ameboid migration models use a cell-focused approach that largely ignores ECM when not acting as a physical barrier
Cell migration is an integral part of many biological functions and pathological conditions, from immune response and wound healing to organ development and cancer metastasis
It should be noted that ameboid cells can exhibit other types of protrusions that are closer to the mesenchymal end of the migration spectrum, i.e., pseudopods.[8]
Summary
Cell migration is an integral part of many biological functions and pathological conditions, from immune response and wound healing to organ development and cancer metastasis. In addition to morphological differences, there are mechanistic differences between the two modes of migration; cytoplasmic pressure gradients drive ameboid migration[12] often in confined settings, whereas mesenchymal migration is driven by actin polymerization and the active maturation and turnover of focal adhesions coupled with actinmyosin contraction[16] across a more spread cell This different mechanism is not entirely distinct from the pressure-driven flowing actin networks of ameboid migration; mesenchymal migrating cells exhibit a retrograde actin flow away from the leading edge and toward the main cell body.[17,18] computational models typically treat different migration modes as entirely distinct for the sake of simplicity and are used to answer specific questions. These modes often exhibit distinct features, making them identifiable, such as the crescent moon shape and gliding motion of keratocytes,[34] but exist in a continuum between mesenchymal and ameboid modes
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
