Testicular germ cell tumors (TGCT) are the most common malignancy affecting males aged 15 to 35. Through unknown mechanisms, they arise from human fetal germ cells that fail to differentiate. They persist in adult testes, forming either a gonocyte-like seminoma, or a differentiated non-seminoma. Several TGF-β/BMP signaling pathway ligands (Activins, NODAL, TGFβ, BMPs) influence mammalian fetal testis development and regulate these germ cells in normal and neoplastic states. Pathway receptors and activated signaling molecules (phosphorylated SMADs) are present in TGCTs, indicating the pathway is active. Aberrant TGF-β pathway signaling during embryonic development is associated with other testicular pathologies. This study used the human gonocyte-like TCam-2 seminoma-derived cell line to investigate Activin–BMP signaling crosstalk in fetal germ cell differentiation and TGCTs. A dual luciferase assay was established by transducing TCam-2 cells with lentivirus to measure BMP4-induced activation of a BMP response element (BRE) and an Activin A-responsive promoter (CAGA). Activin A consistently and dose-dependently antagonized BMP4-induced BRE activation, while BMP4 did not alter Activin A-induced CAGA activation. The effects of Activin A and BMP4 on downstream target gene expression were more complex and target-gene specific. TGFβ signaling requires nuclear transport of phosphorylated SMADs mediated by importin proteins. One of these, IPO5, was recently implicated in BMP signaling; it selectively mediates nuclear localization of the BMP-specific Smads1/5/9 to favor BMP4 target gene activation over Activin/NODAL/TGFβ targets. The abundance of IPO5 in fetal gonocytes and in TCam-2 cells led us to speculate that it selectively promotes BMP signaling. IPO5 knockdown using siRNA impeded BMP4-induced BRE activation and elevated Activin A-induced CAGA activation in TCam-2 cells. Thus, IPO5 levels may be pivotal for determining gonocyte and TGCT responsiveness to the microenvironment.