This project integrates ecological and evolutionary principles to investigate the basis of cancer metastasis, with a particular focus on potential ramifications for cancer progression of tumor cell heterogeneity. That tumor cell heterogeneity can play a critical role in cancer progression is clear, but the underlying evolutionary forces and ecological mechanisms as well as the cell-specific drivers remain important open questions. By using growth competition experiments under controlled conditions using model cell lines (prostate cancer lines PC-3E and GS689), we hope to obtain new insights that can be more broadly applied to understand the effect of tumor cell heterogeneity on tumor evolution. The parental cell line is a heterogenous population containing both cells with epithelial and mesenchymal phenotypes. We conducted a series of competition experiments with the following starting ratio variations of epithelial to mesenchymal: 50:50 (as done in preliminary experiments), 90:10, 75:25, 10:90, 25:75, and 92:8 to test the density-dependent effect on the proliferation of mesenchymal cells in the presence of epithelial cells. This set of experiments suggests a density-dependent ability of GS689 to slow the growth of PC-3E cells. Our observations are consistent with a hypothesis that GS689 cells produce one or more concentration-dependent factors that suppress the growth of the PC-3E cells, resulting in the elimination of PC-3E cells when GS689 cells are present in a high proportion and perhaps retention of GS689 cells via local growth suppression of neighboring PC-3E cells, when GS689 cells start out at a lower proportion. This may help to explain how mesenchymal cells have persisted in the parental population.