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During tissue invasion individual tumor cells exhibit two interconvertiblemigration modes, namely mesenchymal and amoeboid migration. The cellularmicroenvironment triggers the switch between both modes, thereby allowingadaptation to dynamic conditions. It is, however, unclear if thisamoeboid-mesenchymal migration plasticity contributes to a more effective tumorinvasion. We address this question with a mathematical model, where theamoeboid-mesenchymal migration plasticity is regulated in response to localextracellular matrix resistance. Our numerical analysis reveals thatextracellular matrix structure and presence of a chemotactic gradient are keydeterminants of the model behavior. Only in complex microenvironments, if theextracellular matrix is highly heterogeneous and a chemotactic gradient directsmigration, the amoeboid-mesenchymal migration plasticity allows a morewidespread invasion compared to the non-switching amoeboid and mesenchymalmodes. Importantly, these specific conditions are characteristic for in vivotumor invasion. Thus, our study suggests that \emph{in vitro} systems aiming atunraveling the underlying molecular mechanisms of tumor invasion should takeinto account the complexity of the microenvironment by considering the combinedeffects of structural heterogeneities and chemical gradients on cell migration.

Amoeboid-mesenchymal migration plasticity promotes invasion only in complex heterogeneous microenvironments