Prostate cancer is the third most lethal cancer in U.S. men, due to advanced metastatic disease. My dissertation focuses on how the notoriously oncogenic Abl family kinases paradoxically act to suppress the growth and metastasis of prostate cancer. By utilizing a cell-based-model of metastatic prostate cancer, along with genetic depletion/pharmacological inhibition, I have identified signaling pathways dysregulated in the absence of Abl kinase function. These signaling components may provide therapeutic targets for treating prostate cancer.