The dynamics associated with invasion and metastasis, which hallmarks of cancer , and involve collective cell migration by blood or interstitial flow, is poorly understood. ~In the present contribution, we describe a theory to the essence of fluid shear stress (FSS) driven collective motion using the stochastic quantization method . Long range hydrodynamic interactions between cells exhibit complex collective properties whose understanding may be crucial for describing metastasis. ~Theory predicts a shear flow induced migrationof colony of cells characterized by super-diffusive motion. Our findings, suggest a mechanism of shear flow induced directed motion of cancer cells  , and provide the much needed insight into a recent experimental observation concerning the invasion of cancer cells.
The migration behaviors of cancer cells are known to be heterogeneous. However, the interplay between the adhesion interactions, dynamical shape changes and fluid flows in regulating cell migration heterogeneity and plasticity during cancer metastasis is still elusive. To further quantitative understanding of cell motility and morphology, we develop a theory using stochastic quantization method that describes the role of biophysical cues in regulating diverse cell motility. We show that the cumulative effect of time dependent adhesion interactions that determine the structural rearrangements and self-generated force due to actin remodeling, dictate the super-diffusive motion of mesenchymal phenotype in the absence of flow. Interstitial flows regulate cell motility phenotype and promote the amoeboid over mesenchymal motility through adhesion interactions. Cells exhibit a dynamical slowing down of collective migration, with a decreasing degree of super-diffusion. Our findings, suggest a mechanism of Interstitial flow induced directed motion of cancer cells through adhesion , and provide the much needed insight into a recent experimental observation concerning the diverse motility of breast cancer cells.
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dynamics associated with invasion and metastasis, which hallmarks of cancer , and involve collective cell migration by blood or interstitial flow, is poorly understood. ~In the present contribution, we describe a theory to the essence of fluid shear stress (FSS) driven collective motion using the
migration behaviors of cancer cells are known to be heterogeneous. However, the interplay between the adhesion interactions, dynamical shape changes and fluid flows in regulating cell migration heterogeneity and plasticity during cancer metastasis is still elusive. To further quantitative understanding of cell motility and morphology, we develop a theory using
R
. Long range hydrodynamic interactions between cells exhibit complex collective properties whose understanding may be crucial for describing metastasis. ~Theory predicts a shear flow induced migrationof colony of cells characterized by
that describes the role of biophysical cues in regulating diverse cell motility. We show that the cumulative effect of time dependent adhesion interactions that determine the structural rearrangements and self-generated force due to actin remodeling, dictate the
R
motion.
motion of mesenchymal phenotype in the absence of flow. Interstitial flows regulate cell motility phenotype and promote the amoeboid over mesenchymal motility through adhesion interactions. Cells exhibit a dynamical slowing down of collective migration, with a decreasing degree of super-diffusion.
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shear
Interstitial
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through adhesion
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invasion of
diverse motility of breast