Prostate cancer is the most commonly diagnosed malignancy for men in the United States. Fortunately, radiation and prostatectomy are curative in the majority of disease cases. However, metastatic prostate cancer, the lethal form of the disease, has a life expectancy of approximately five years. Identification of factors associated with this transition to metastatic disease are crucial for future therapies. One potential factor is the SSX gene family, a family transcription factors shown to be aberrantly expressed in cancers and associated with the epithelial to mesenchymal transition (EMT). In order to target SSX in prostate cancer, we must first fully understand it. Thus, main aims of the following thesis are threefold: characterization of SSX expression, characterization of SSX function, and finally characterization of SSX specific CD8+ T cells responses. In this thesis, we have identified SSX2 as the predominant SSX family member expressed in prostate cancer, and found its expression in circulating tumor cells (CTCs), and metastatic cDNA samples. Further, we examined SSX2 function in prostate cancer through knockdown and overexpression in prostate cancer cell lines. While overexpression had little effect on morphology or gene transcript changes, knockdown of SSX2 resulted in an epithelial morphology, increased cell proliferation, increased expression of genes involved in focal adhesion, decreased anchorage independent growth, increased invasion, and increased tumorigenicity in vivo. We concluded from these findings that SSX2 expression in prostate cancer is not a driver of EMT, but is involved in processes associated with EMT including loss of focal adhesion that may related to tumor cell dissemination. Finally, we assayed patients for presence of SSX specific CD8+ T cells and SSX expressing CTCs (n=15). We found patients with SSX expressing CTCs also possessed SSX specific CD8 T cells (6/15), while other patients possessed SSX specific CD8+ T cells but not SSX CTCs (9/15). We sought to determine the cause of this duality, and further characterize SSX specific CD8+ T cells. Finally, concluded that checkpoint molecule regulation was unlikely to be the cause of this duality, but the expression of Th1 biased cytokines may cause this duality.