WNT signaling exerts pleiotrophic influences throughout development. We show using immunohistochemical analysis that WNT signaling is active in the adult human testis. Nuclear-localised beta-catenin (CTNNB1), indicative of active canonical WNT signaling, is restricted to post-meiotic germ cells, specifically round spermatids. Because of the known links between dysregulated WNT signaling and cancer, we assessed the potential for WNT signaling in a human germ cell tumour (seminoma) line, TCam-2. Quantitative (Q)-RTPCR analysis detected WNT ligands (WNT2B, 4, and 5A), receptors (FZD2, 5, 6, 7, and LRP6), and downstream signaling molecules (APC, AXIN2, and CTNNB1). However, we detected no nuclear CTNNB1 in either TCam-2 cells, or in carcinoma in situ (CIS) or seminoma tumours. Intriguingly, exposure of TCam-2 seminoma cells to conditioned media containing the canonical signaling ligand WNT3A for 1, 4, and 7 hours, resulted in rapid elevation of nuclear CTNNB1 (within 1 hour), measured as significantly increased compared to controls. To identify the functional outcome of WNT activity, we exposed the TCam-2 cells to a suite of WNT signaling agonists and antagonists, then measured cell growth (cell numbers) and viability (propidium iodide incorporation) outcomes. These parameters were not affected in the presence of the receptor antagonist DKK, suggesting that there is little autocrine WNT signaling in TCam-2 cultures. However, when either canonical (WNT3A) or non-canonical (WNT5A) WNT signaling was activated by exogenous ligand, we observed a significant increase in cell numbers and viability following 5 and 10 days of culture, compared to untreated controls. These data indicate that seminoma cells respond to WNT pathway activation, however a critical question this study raises is what factors may be acting to inhibit this signaling activation in vivo.