CEBPB-high dormant tumor cells drive immune evasion [RNA-Seq]
Triple negative breast cancer (TNBC) poorly responds to immune checkpoint blockade (ICB) therapy. Dormant tumor cells are recognized as immunotherapy-resistant reservoirs, potential leading to tumor relapse, highlighting the importance to elucidate the mechanisms underlying immunotherapy resistance. Herein, we demonstrated that dormant tumor cells were resistant to ICB therapy and occupied an immunosuppressive niche with enhanced tumor-associated macrophages (TAMs) and decreased CD8+T cells infiltration in mouse TNBC allografts via a label-retention system. CEBPB was highly expressed in dormant tumor cells and maintained tumor dormancy by transcriptionally activating cell cycle negative regulators like CCNG2 and p27. Overall design: To investigate which genes were regulated by CEBPB in triple negative breast cancer, we transfected 4T07 cell lines with either pLenti-CMV-MCS or pLenti-CMV-Cebpb by lentivirus. Stable tracfected cells were selected by puromycin.We extracted RNA from each group with three biological replicates. We performed gene expression profiling assay using data obtained from RNA-seq of 6 samples (two groups with three biological replicates per group). Comparative gene expression profiling analysis of RNA-seq data for OE-Control and OE-Cebpb