Oxidative Stress-Induced Immunogenic Cell Death Enhances Whole-Cell Vaccine Efficacy in a Syngeneic Pancreatic Cancer Model
RNA sequencing was performed to characterize transcriptional changes induced by sub-lethal oxidative stress in murine pancreatic cancer cells. Panc02 cells were exposed to low-dose hydrogen peroxide and compared with untreated controls. Differential gene expression analysis revealed extensive transcriptomic remodeling, including induction of stress-response programs, inflammatory and antiviral signaling pathways, chemokines involved in immune cell recruitment, and components of the MHC class I antigen presentation machinery. These data define the RNA-level response of pancreatic cancer cells to oxidative stress and provide insight into mechanisms by which stress conditions enhance tumor cell immunogenicity. Overall design: Murine Panc02 pancreatic cancer cells were cultured in vitro and divided into two conditions: untreated control and oxidative stress treatment with hydrogen peroxide. Total RNA was extracted from biological replicates in each group and used to generate poly(A)+ RNA-seq libraries. Libraries were sequenced using paired-end Illumina sequencing. Reads were quality-controlled, aligned to the mouse reference genome, and quantified at the gene level. Differential expression analysis was conducted to identify genes and pathways altered by oxidative stress.