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Background   UEV1A  encodes a ubiquitin-E2 variant closely associated with tumorigenesis and metastasis, but its underlying mechanism in promoting metastasis remains to be investigated.    Methods  In this study, we experimentally manipulated  UEV1A  and  CT45A  gene expression and monitored their effects on cancer-related gene expression, cell migration and the signal transduction cascade.    Results  It was found that  UEV1A  overexpression induces  CT45A  family gene expression in breast cancer cells. Indeed, ectopic expression of  UEV1A  was sufficient to induce  CT45A  and its downstream genes involved in tumorigenesis, epithelial-mesenchymal transition (EMT), stemness and metastasis, and to promote cell migration and EMT signaling. Consistently, depletion of CT45A abolished the above effects, indicating that CT45A is a critical downstream effector of Uev1A. The Uev1A-induced cell migration and EMT signaling was dependent on AKT but independent of NF-κB, indicating that CT45A acts downstream of the AKT pathway.    Conclusions  Based on previous reports and observations in this study, we propose that the Ubc13-Uev1A complex activates AKT through K63-linked polyubiquitination, which leads to enhanced  CT45A  expression, stimulated cell migration and EMT signaling in breast cells. Since similar effects were also observed in a colorectal cancer cell line, the Ubc13/Uev1A-AKT-CT45A axis may also promote tumorigenesis and metastasis in other tissues.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12885-021-08750-3.

Uev1A promotes breast cancer cell migration by up-regulating CT45A expression via the AKT pathway