Targeting IGF2BP1 reverses immune evasion in CTL-enriched pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) remains poorly responsive to immune checkpoint therapy. To investigate tumor-intrinsic immune evasion mechanisms, we performed RNA-sequencing of the basal-like PANC-03.27 PDAC cell line following IGF2BP1 knockdown using pooled siRNAs. Transcriptome profiling revealed induction of interferon-? signaling and downregulation of curated IGF2BP1 target transcripts, consistent with a conserved immunoregulatory program. Gene set enrichment analysis and STAT reporter assays confirmed activation of JAK/STAT-dependent pathways. These datasets provide a resource for understanding IGF2BP1-mediated transcriptional regulation in PDAC and for identifying potential targets to enhance anti-tumor immune responses. Overall design: PANC-03.27 cells were transfected with an IGF2BP1-directed siRNA pool (30nM) or control siRNAs 72h before RNA isolation by TRIzol to determined IGF2BP1-dependent changes in gene expression using poly(A) enriched bulk RNA-sequencing.