Abstract 

Collective cell migration is an essential process during development, tissue homeostasis, and cancer metastasis. In the early stages of metastasis in solid tumors, cancer cells break away from the primary tumor and migrate through the surrounding stromal tissue, which is primarily comprised of collagen-I networks. Despite the importance of this process, the mechanisms of collective cell migration in stroma-like environments are poorly understood. Our recent work has revealed a mechanical feedback loop between groups of cells and collagen networks that drives spontaneously persistent collective migration without any apparent intrinsic cell polarity. Combining theory and experiments, we show that collagen network viscoelasticity is essential for this feedback, and that modulating collagen network rheology results in reduced migration persistence. Currently, we are investigating mechanisms of collective migration and cell patterning in the mammalian intestinal epithelium. We are particularly interested in understanding the relationship between Wnt signaling and cell-cell adhesions via the common mediator β-catenin.