In many types of cancer c-Src signaling is greatly increased, therefore, linking to advanced malignancy and poor prognosis. Our studies have shown that secreted c-Src phosphorylates TIMP-2 which impacts on MMP-2 activity. We have also shown that blocking e-Src with anti-c-Src antibodies have an inhibitory effect on TIMP-2 phosphorylation and its interaction with MMP-2. In addition, we utilize cell-based, transcriptomic, proteomic and phosphoproteomic approaches to understand the extracellular and intracellular pathways involved. Our goal is to determine the broader role of e-Src in tumor biology and establish e-Src as a therapeutic target in cancer cells.