UNC93B1 promotes pancreatic cancer progression through modulation of cGAS–STING signaling

By integrating multi-omics data, including GWAS and spatial transcriptomics, this study systematically defines a pivotal role for UNC93B1 in PDAC progression. Our findings demonstrate that UNC93B1 is associated with an immunosuppressive TME and facilitates metastatic spread, potentially through inhibiting the cGAS-STING-mediated innate immunity pathway. The strong correlation between UNC93B1 overexpression and adverse clinical outcomes underscores its potential as a dual diagnostic biomarker and therapeutic target. This work not only provides a mechanistic foundation for novel precision immunotherapies in PDAC but also establishes a robust methodological paradigm for multi-omics-driven discovery in oncology.