Localization of β-catenin in the cell is a key determinant in its decision to function as a critical mediator of cell adhesion at the surface or a transcription activator in the nucleus. SYT-SSX2 is the fusion product of the chromosomal translocation, t (X; 18)(p11. 2; q11. 2), which occurs in synovial sarcoma, a soft tissue tumor. SYT-SSX2 is known to associate with chromatin remodeling complexes and is proposed to be involved in controlling gene expression. We report that SYT-SSX2 plays a direct role in β-catenin regulation. When expressed in mammalian cells, SYT-SSX2-induced β-catenin recruitment to the nucleus. Interestingly, known target genes of canonical Wnt were not activated as a result of SYT-SSX2 expression, nor was the nuclear localization of β-catenin due to one of the signaling pathways normally implicated in this event. β-Catenin accumulation in the nucleus led to the formation of a transcriptionally active nuclear complex that contained SYT-SSX2 and β-catenin. More importantly, depletion of SYT-SSX2 in primary synovial sarcoma cells resulted in loss of nuclear β-catenin signal and a significant decrease in its signaling activity. These results unravel a novel pathway in the control of β-catenin cellular transport and strongly suggest that SYT-SSX2 contributes to tumor development, in part through β-catenin signaling.