BAP31 Facilitates TGF-β Trafficking and Secretion and Promotes Dendritic Cell Dysfunction in Cervical Cancer

Cervical cancer remains one of the major gynecological malignancies worldwide, with tumor immune evasion playing a critical role in disease progression. Although accumulating evidence has implicated BAP31 in tumor progression and immune regulation, its role in immune evasion in cervical cancer remains poorly understood. In this study, we found that BAP31 was significantly upregulated in cervical cancer tissues and that elevated BAP31 expression was associated with poor patient prognosis. Functional assays demonstrated that BAP31 silencing restored the immune activity of dendritic cells. Mechanistically, BAP31 was found to regulate TGF-β at the post-transcriptional level and to facilitate its transport from the endoplasmic reticulum to the Golgi apparatus through an interaction involving the Asn-381 residue, thereby affecting its intracellular maturation and extracellular secretion. Additional functional analyses showed that exogenous TGF-β impaired dendritic cell maturation and migration while enhancing phagocytic activity. Collectively, these findings indicate that BAP31 regulation of TGF-β contributes to dendritic cell dysfunction and the establishment of an immunosuppressive microenvironment in cervical cancer.