Loss of ZNF408 Attenuates STING-mediated Immune Surveillance in Breast Carcinogenesis

In this study, we find that ZNF408 physically interacts with the SETD1A/COMPASS complex to promote H3K4me3 deposition and transcription activation. We characterize the genomic, epigenomic, and transcriptomic landscapes of ZNF408 and identify the genome-wide target genes of ZNF408. We establish a functional link between ZNF408 and the cGAS/STING1-mediated innate immune response. We investigate the clinicopathological significance of the ZNF408-SETD1A -STING1 axis in breast cancer and propose that down-regulation of ZNF408 is linked to immune escape in breast carcinogenesis.