Abstract
JUNB and JUND are two transcriptional factors (TFs) of increased interest in cancer, regulating the expression of genes associated with survival, proliferation, differentiation, migration, invasion, angiogenesis, adhesion, apoptosis, and cell cycle regulation. Together with c-JUN, they constitute the JUN family of TFs, acting as downstream effectors of the MAPKs, with established roles in carcinogenesis, disease progression, metastasis, and therapy resistance. Their phosphorylation leads to the formation of dimeric complexes with other TFs (from the JUN, FOS, or ATF families), thereby assembling the AP-1 complex, which exerts multifaceted influences on both normal and cancerous cells. JUNB and JUND are credited with both tumor-suppressing and oncogenic roles, since the outcome of their activation relies on the specific cancer type, disease stage, intracellular localization, and the expression of interacting cofactors. This narrative review explores the current understanding of JUNB and JUND roles within urological cancers (prostate, bladder, renal, and testicular cancer) as these malignancies, while distinct, share common genetic and/or environmental risk factors and varying degrees of androgen receptor (AR) dependency. The study discusses commonalities and differences in the expression patterns, mechanisms, and clinical implications of JUNB and JUND across urological cancers, thus highlighting their potential as prevention, diagnosis, prognosis, and treatment targets.