  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.
Mesenchymal cells are more persistent and diffusive compared to amoeboid cells.
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.
