Directed cell movement, chemotaxis, is a part of normal physiological processes such as wound healing, immune response and embryogenesis. However, this pathway can also be hijacked during tumor development, allowing cancer cells to metastasize. In this talk, I will discuss an ongoing collaboration in modeling the regulation of actin cytoskeleton in mammary carcinoma motility. I will survey results from a temporal ODE model of the regulation of cofilin, an actin regulatory protein that is upregulated in invasive carcinoma. Second, I will present a spatio-temporal model of actin growth to look at the collective effects of two actin regulatory proteins. At the end, I will motivate our current effort in studying invadopodia, a dynamic actin-based structure that allows cancer cell to dig through its surrounding environment. This work is done jointly with John Condeelis (Albert Einstein College of Medicine) and Leah Edelstein-Keshet (University of British Columbia).