Divergent Roles of C/EBPβ Isoforms LAP and LIP in Shaping T Cell Dysfunction and Tumor Progression in Triple‐Negative Breast Cancer

C/EBPβ, a member of the CCAAT/enhancer‐binding protein (C/EBP) family of transcription factors, is implicated in monocyte differentiation, inflammation, and cancer progression. However, the distinct roles of its transcriptional activator (LAP) and repressor (LIP) isoforms in triple‐negative breast cancer (TNBC) pathogenesis remain unclear. In this study, we demonstrate that LAP critically promotes TNBC growth, whereas single‐cell RNA sequencing reveals that LAP overexpression drives CD8 + T cell exhaustion, whereas LIP primarily modulates CD4 + T cell function. Integrative ATAC‐seq, ChIP‐seq, and RNA‐seq analyses further show that LAP enhances chromatin accessibility and activates the EGFR signaling pathway, whereas LIP exerts minimal effects on TNBC phenotypes. These findings establish LAP as a key oncogenic driver in TNBC and unveil its immunosuppressive role in shaping the tumor microenvironment, offering potential therapeutic targets for TNBC treatment.