  Mechanics and biochemical signaling are both often deregulated in cancer,
leading to cancer cell phenotypes that exhibit increased invasiveness,
proliferation, and survival. The dynamics and interactions of cytoskeletal
components control basic mechanical properties, such as cell tension,
stiffness, and engagement with the extracellular environment, which can lead to
extracellular matrix remodeling. Intracellular mechanics can alter signaling
and transcription factors, impacting cell decision making. Additionally,
signaling from soluble and mechanical factors in the extracellular environment,
such as substrate stiffness and ligand density, can modulate cytoskeletal
dynamics. Computational models closely integrated with experimental support,
incorporating cancer-specific parameters, can provide quantitative assessments
and serve as predictive tools toward dissecting the feedback between signaling
and mechanics and across multiple scales and domains in tumor progression.
