GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE304nnn/GSE304428/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE304428GEOGSEfalseDMAP1 promotes lung cancer progression by maintaining replication fork stability and suppressing IFN signaling-mediated anti-tumor immunity [RNA-seq]Despite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of tumor progression. Functional studies showed that loss of DMAP1 exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, loss of DMAP1 causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating tumor-intrinsic immune signaling and enhancing anti-tumor immune response during cancer cell growth. Clinical data analyses revealed that high DMAP1 expression is associated with reduced immune infiltration, a “cold” tumor microenvironment, and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1's function in lung cancer development and offer a scientific basis for designing novel treatment approaches.2026/06/24GSE304428GSM9150431GSM9150430GSM9150428GSM9150429GSM9150426GSM915042724247304428Mus musculus[41904944]